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90 publications mentioning mmu-mir-130a

Open access articles that are associated with the species Mus musculus and mention the gene name mir-130a. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 354
Other miRNAs from this paper: hsa-mir-130a
After correction for multiple testing, we identified 31 up-regulated and 13 down-regulated proteins in the 32Dcl3 miR-130a clone, and 19 up-regulated and 15 down-regulated proteins in Kasumi-1 cells, following miR-130a inhibition (q < 0.01). [score:15]
In the 32Dcl3 clone, putative targets were more up-regulated than the remaining quantified proteins following miR-130a inhibition, and three significantly derepressed proteins (NFYC, ISOC1, and CAT) are putative miR-130a targets with good RAIN scores. [score:10]
We also created a network including inferred, putative neutrophil miR-130a targets and identified the transcription factors Myb and CBF-β as putative miR-130a targets, which may regulate the primary granule proteins MPO and PRTN3 and other proteins differentially expressed following miR-130a inhibition in the 32Dcl3 clone. [score:10]
The significantly down-regulated Smarcb1 associates with Smarcd2, which is a predicted miR-130a target and down-regulated, although not significantly, in this study. [score:9]
We identified subsets of the murine and human neutrophil proteomes significantly regulated by miR-130a, which likely represent a mixture of direct targets, including NFYC, ISOC1, and CAT, and mainly indirect miR-130a targets. [score:8]
We found potential targets to be more up-regulated after miR-130a inhibition for the 32Dcl3 miR-130a clone (Kolmogorov–Smirnov test, p-value = 0.018) as demonstrated by the right shift of the curve showing higher M/H ratios. [score:8]
Linking these to putative miR-130a targets, we provide an association network of potential direct and indirect miR-130a targets that expands our knowledge on the role of miR-130a in neutrophil development and is a valuable platform for further experimental studies. [score:8]
CBF-β is up-regulated 1.35-fold (although not statistically significant) in the 32Dcl3 miR-130a clone following miR-130a inhibition and a candidate upstream regulator of three proteins within the regulated subset: MPO, IL-2Ra (Ingenuity Pathway analysis) and proteinase 3 (PRTN3, author observations, unpublished). [score:8]
If Myb is up-regulated following inhibition of miR-130a, this could lead to the observed increases of its targets, the primary granule proteins MPO [49] and PRTN3 [50] (Fig.   4). [score:8]
We demonstrated that substantial inhibition of miR-130a affects the overall expression of predicted target proteins in the murine neutrophil mo del system. [score:7]
These fold changes are included in the network to also indicate the observed direction of strongly predicted targets quantified but not significantly regulated within the data set In murine cells, RAIN does not identify Smad4 as a miR-130a target. [score:7]
Based on these analyses, we identified Myb and CBF-β as putative direct miR-130a targets and potential regulators of the primary granule proteins MPO and PRTN3 following miR-130a inhibition in the 32Dcl3 miR-130a clone. [score:7]
miR-130a is highly expressed during early neutrophil development and regulates target proteins important for this process. [score:7]
We showed that miR-130a suppresses expression of Smad4 and thereby reduces sensitivity to TGF-β1 -induced growth inhibition [9]. [score:7]
These fold changes are included in the network to also indicate the observed direction of strongly predicted targets quantified but not significantly regulated within the data setIn murine cells, RAIN does not identify Smad4 as a miR-130a target. [score:7]
RAIN does identify a weak interaction, although below the network cut-off, between Smad4 and NFYC, which is significantly up-regulated upon miR-130a inhibition. [score:6]
Of these three only MPO and PRTN3 were identified in the Kasumi-1 experiment, and only PRTN3 was borderline significantly up-regulated (q = 0.0113), probably reflecting the greater degree of miR-130a inhibition by anti-miR-130a-LNA observed in the 32Dcl3 miR-130a clone (Additional file 3: Figure S2). [score:6]
Three derepressed proteins (NFYC, ISOC1, and CAT) with miR-130a association probabilities within the top 20 % were found in the 32Dcl3 miR-130a clone and one (Phosphatidylinositide phosphatase SAC1, SACM1L) in Kasumi-1 cells (Fig.   2), indicating that most of the de-regulated proteins are either indirectly regulated by miR-130a or bona fide miR-130a targets not found by RAIN. [score:6]
Red: up-regulated >0.3 (log2 ratio) upon miR-130a inhibition. [score:6]
Fig. 4 RAIN networks of potential miR-130a targets (with miR-130a association probabilities in the top 20 %) and differentially regulated proteins identified for the 32Dcl3 miR-130a clone following miR-130a inhibition. [score:6]
Green: down-regulated < −0.3 (log2 ratio) upon miR-130a inhibition. [score:6]
Using pulsed stable isotope labelling of amino acids in cell culture and mass spectrometry for protein identification and quantitation, we found 44 and 34 proteins that were significantly regulated following inhibition of miR-130a in a miR-130a -overexpressing 32Dcl3 clone and Kasumi-1 cells, respectively. [score:6]
We identified important myeloid regulatory proteins, such as Myb and Core -binding factor beta (CBF-β), as putative direct miR-130a targets. [score:5]
We demonstrate that inhibition of miR-130a with an anti-miR-130a oligonucleotide in a miR-130a -overexpressing 32Dcl3 clone and in Kasumi-1 cells results in significant changes in the levels of 44 out of 2092 proteins and 34 out of 1238 proteins, respectively. [score:5]
TargetScan identifies Smad4 as a human miR-130a target with two seed matches (MREs) in the Smad4 3′ UTR. [score:5]
We found that putative miR-130a target proteins are more induced than the remaining proteins quantified in the 32Dcl3 miR-130a clone following miR-130a inhibition. [score:5]
The murine myeloblast-derived cell line 32Dcl3 was stably transfected with a miR-130a -expressing plasmid, resulting in a clone over -expressing miR-130a. [score:5]
Not much is known about ISOC1, also significantly derepressed by miR-130a inhibition and a highly predicted miR-130a target, other than that it associates with peroxisomes, has enzymatic activity, and may promote cell growth [53, 54]. [score:5]
This confirms that there is an overall greater effect of inhibiting miR-130a in cells from the 32Dcl3 miR-130a clone where the free miR-130a pool is much more reduced (~31 fold reduction) than in the Kasumi-1 cell line (~2.3 fold reduction) upon LNA -mediated inhibition (Additional file 3: Figure S2). [score:5]
The same MREs are also found in the murine Smad4 3′ UTR, but presumably other factors of the TargetScan algorithm prevent its prediction of murine Smad4 as a miR-130a target since murine and human miR-130a are identical. [score:5]
miR-130a also represses appropriate cell cycle exit and secondary granule protein expression by targeting C/EBPε in neutrophil precursors [9, 11]. [score:5]
The proteins identified in MS were compared with the top 20 % best scoring RAIN association probabilities for miR-130a to a) find potential miR-130a targets among the quantified proteins for the two cell lines, and to b) identify potential miR-130a target proteins for the miR-130a association network that might associate with proteins within the regulated protein subset found for the 32Dcl3 miR-130a clone. [score:5]
Finally, we constructed miR-130a target protein networks including the proteins identified in this study in order to find pathways affected by miR-130a in the context of neutrophil development. [score:4]
A Kolmogorov-Smirnov test of equality between distributions results in the following: p-value = 0.018 for the comparison between M/H ratios of proteins with good RAIN scores and the M/H ratios of proteins without scores; p-value = 0.042 for the M/H ratios of proteins with good RAIN scores and the M/H ratios of all remaining proteinsSecondly, we used RAIN to determine potential miR-130a targets within the subsets of significantly regulated proteins. [score:4]
First, we used RAIN to determine whether changes in protein levels could be directly attributed to the inhibition of miR-130a. [score:4]
This indicates that, in addition to transcription factors, miR-130a may target other types of transcriptional regulators as well as metabolic processes in neutrophil precursors. [score:4]
Together, these results provide significant insight into multiple miR-130a-regulated proteins and emphasize its important regulatory role in neutrophil development. [score:4]
A Kolmogorov-Smirnov test of equality between distributions results in the following: p-value = 0.018 for the comparison between M/H ratios of proteins with good RAIN scores and the M/H ratios of proteins without scores; p-value = 0.042 for the M/H ratios of proteins with good RAIN scores and the M/H ratios of all remaining proteins Secondly, we used RAIN to determine potential miR-130a targets within the subsets of significantly regulated proteins. [score:4]
dk/resources/rain/], to identify potential direct miR-130a targets among the proteins found within our two studies (see for details). [score:4]
We have previously experimentally identified Smad4 as a direct miR-130a target in murine cells [9]. [score:4]
This complex plays an important role in cell cycle progression [52] and may thus be regulated in neutrophil precursors by miR-130a targeting two of its subunits. [score:4]
CBF-β, Myb, and miR-130a are co-expressed in early myeloid precursors, suggesting that miR-130a may have a buffer effect on their protein levels ([48, 51] and unpublished data). [score:3]
In summary, these and other interactions identified here can form the basis for further experimental identification of miR-130a regulation in neutrophil development extending further than just single miR-130a–mRNA interactions. [score:3]
The level of miR-130a inhibition correlated with the impact on protein levels. [score:3]
miR-130a Neutrophils pSILAC Quantitative proteomics RAIN miRNA target network Neutrophils are the most abundant leukocytes in human blood. [score:3]
CBF-β is a highly predicted miR-130a target (top 20 %). [score:3]
Fig. 2The intensities in MS as a function of log2 fold changes in protein expression between the anti–miR-130a-LNA and scrambled-LNA conditions for the 32Dcl3 miR-130a clone (a) and the Kasumi-1 cells (b). [score:3]
To identify additional potential regulatory networks involving miR-130a, we constructed association networks for the subset of 44 regulated proteins found for the 32Dcl3 miR-130a clone. [score:3]
pSILAC approach for identification of myeloid miR-130a target proteins. [score:3]
The Kasumi-1 cell line is derived from an acute myeloid leukemia patient with t(8;21)(q22;q22) chromosomal translocation and has a 2.5-fold higher endogenous expression of miR-130a than the level found in primary myeloblasts and promyelocytes isolated from normal human bone marrow [9]. [score:3]
Therefore, it cannot be excluded that certain interesting miR-130a targets will be missed using RAIN due to this restriction in the underlying databases. [score:3]
NFYC is a predicted miR-130a target, but the effect of miR-130a might also be mediated by Smad4 or one of its other associated network proteins such as its heterotrimeric transcription factor complex partner NFYA. [score:3]
We used RAIN, a novel database for miRNA–protein and protein–protein interactions, to identify putative miR-130a targets. [score:3]
Fig. 3The cumulative distributions of M/H ratios of proteins with good RAIN scores (top 20 %, green), all remaining proteins (black), and proteins without RAIN scores (orange) as a function of log2 M/H fold changes in protein expression between the anti-miR-130a-LNA (M) and scrambled-LNA (H) conditions for the 32Dcl3 miR-130a clone. [score:3]
Three significantly induced proteins, nuclear transcription factor Y, gamma (NFYC), isochorismatase domain containing 1 (ISOC1), and catalase (CAT), are putative miR-130a targets with good scores in RAIN (RNA–protein Association and Interaction Networks) [http://rth. [score:3]
The murine myeloblast-derived cell line 32Dcl3 (ATCC® CRL-11346) was stably transfected with the expression plasmid pEGP-miR-130a (Cell Biolabs) as described previously [9]. [score:3]
Myb is a predicted miR-130a target but was not identified in either cell line. [score:3]
The last miR-130a target with a good RAIN score and significantly derepressed protein in the 32Dcl3 miR-130a clone is CAT. [score:3]
These two targets for miR-130a were suggested by in silico prediction algorithms based on conservation across species, sequence complementarity, and other miRNA–mRNA binding properties [12, 13]. [score:3]
We transiently transfected the 32Dcl3 miR-130a clone and Kasumi-1 cells with an inhibitory LNA probe against miR-130a (anti-miR-130a-LNA) or a scrambled-LNA (mock transfection). [score:3]
Identification of miR-130a targets in the neutrophil proteome. [score:3]
miR-130a expression in the 32Dcl3 and Kasumi-1 cell lines. [score:3]
Combining the significantly regulated murine protein subset with high-scoring putative miR-130a targets from the RAIN database in an interaction network, we identified subsets of proteins with potential roles in downstream miR-130a regulation relevant for further experimental investigation. [score:3]
The major miR-130a network includes the transcriptional activator Myb, which is more highly expressed in early neutrophil precursors compared to more mature cells [48]. [score:2]
We compared the fold changes of potential miR-130a target proteins with a good RAIN score (top 20 %) to those of proteins without scores (Fig.   3). [score:2]
A. H/M ratios of significantly regulated proteins in the 32Dcl3 miR-130a clone also identified and quantified for the Kasumi-1 cell line. [score:2]
Therefore, both CBF-β and Myb are potential direct miR-130a targets worth investigating further. [score:2]
miR-130a is highly expressed in early neutrophil precursors (myeloblasts and promyelocytes) compared to more mature precursors [9, 10]. [score:2]
Proteins differentially regulated by miR-130a were determined based on statistical significance rather than a fold change cut-off. [score:2]
We have experimentally identified miR-130a-regulated proteins within the neutrophil proteome. [score:2]
B. H/M ratios of significantly regulated proteins in the Kasumi-1 cell line also identified and quantified for the 32Dcl3 miR-130a clone. [score:2]
This resulted in a major miR-130a network as well as several minor, disconnected networks (Fig.   4). [score:1]
As most of the associations come from prediction algorithms, we chose the top 20 % highest scoring associations, which consist of 678 predictions, 5 experiments, and 6 text-mining interactions for miR-130a in mice. [score:1]
Proteins are represented by crosses (miR-130a association probability in top 20 %) or dots (miR-130a association probability below top 20 % or no score). [score:1]
Assignment of p-values to ratios (shown for the 32Dcl3 miR-130a clone). [score:1]
The sequences of murine and human miR-130a-3p (miR-130a) are identical. [score:1]
This corresponds well with observed effects of miR-130a on proliferation and cell cycle in immature neutrophil cells [9, 11]. [score:1]
At this point, the effect of miR-130a is reflected by differences between M and H proteins while light (L) proteins have all been synthesized prior to interference with the free miR-130a pool. [score:1]
This 32Dcl3 miR-130a clone was cultured in SILAC medium consisting of RPMI medium without arginine, lysine, and glutamine (PAA Cell Culture Company), 10 % dialysed FBS (Gibco), 100 U/mL penicillin and 100 μg/mL streptomycin (Gibco), 1 ng/mL murine IL-3 (Sigma-Aldrich), 1 % GlutaMAX™-1 (Gibco), and 0.2 mg/mL proline (Sigma-Aldrich) to avoid arginine-to-proline conversion [24]. [score:1]
a Cells grown in L medium were transfected with anti-miR-130a-LNA or scrambled-LNA (mock-transfection) and transferred to M or H SILAC-medium, respectively. [score:1]
This has previously been shown to be a good mo del for investigating the effect of miR-130a on specific target proteins [9, 11]. [score:1]
Other proteins that interact with this protein subset with protein-protein association probabilities above 0.7 and which have miR-130a association probabilities within the top 20 % were also included. [score:1]
Each protein was assigned a miR-130a association probability by mapping to RAIN [http://rth. [score:1]
For pSILAC, the 32Dcl3 miR-130a clone was grown in SILAC L medium for six days and subsequently washed twice with phosphate-buffered saline (PBS) to eliminate traces of L amino acids. [score:1]
Our aim was to evaluate the effect of miR-130a on the proteome at the time of neutrophil maturation when miR-130a expression is at its peak (myeloblasts and promyelocytes) [9]. [score:1]
Expression of miR-130a following transfection with an anti-miR-130a-LNA or scrambled-LNA of the 32Dcl3 miR-130a clone for 48 h (left) and Kasumi-1 cells for 72 h (right) measured by real-time PCR. [score:1]
Impact of miR-130a on protein output. [score:1]
Cells (5x10 [6]/condition) were then transfected with anti–miR-130a-LNA or scrambled-LNA (Exiqon) through electroporation using the AMAXA nucleofection system (program E-032) according to the manufacturer’s recommendations and transferred to M (anti–miR-130a-LNA) or H (scrambled-LNA) medium for approximately 48 h. Similarly, Kasumi-1 cells (human myeloblast cell line derived from a patient with acute myeloblastic leukemia, ATCC® CRL-2724) were grown in normal medium (RPMI1640 (Gibco), 20 % FBS (Gibco), 100 U/mL penicillin and 100 μg/mL streptomycin (Gibco)), washed twice with PBS before transfection (program C-23) with anti–miR-130a-LNA or scrambled-LNA (Exiqon) and switched to M or H SILAC medium, respectively, for approximately 72 h. The SILAC medium used for Kasumi-1 cells was identical to the 32Dcl3 SILAC medium except 20 % dialysed FBS was used and no IL-3 was added. [score:1]
After 48 h (32Dcl3 miR-130a clone, doubling time ~18–20 h) or 72 h (Kasumi-1, doubling time ~40 h) of pulse labelling, cells were washed, combined 1:1, and lysed. [score:1]
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[+] score: 315
We show that miR-130a is expressed in cardiomyocytes and when over-expressed during embryonic development, results in a down-regulation of FOG-2 protein levels and structural heart defects similar to those seen in mice deficient in FOG-2, thus suggesting that it may play a role in regulating cardiac development. [score:11]
Given our observation that miR-130a expression is dynamically regulated in the heart during embryonic development, miR-130a may also play a role in regulating cardiac development, at least in part by translational regulation of FOG-2, mediated through a conserved site located in the FOG-2 3′UTR. [score:10]
Mutation of the predicted miRNA target site within the FOG-2 UTR or blocking miR-130a relieves this translational inhibition. [score:8]
Given its cardiac expression and target site conservation, miR-130a is an attractive candidate as a potential regulator of FOG-2 mRNA translation and thus is the focus of the remainder of this report. [score:8]
To express miR-130a in COS-7 fibroblasts, we engineered a mammalian expression vector containing the CMV promoter driving expression of the miR-130a precursor stem loop structure (Fig. 4C). [score:7]
To test if expression of miR-130a would repress translation of our reporter construct containing the FOG-2 3′ UTR, we co -transfected COS-7 fibroblasts with our miR-130a expression vector and our FOG-2 UTR reporter. [score:7]
It was our hypothesis that overexpression of miR-130a in the embryonic heart would lead to similar defects by inhibiting translation of FOG-2 mRNA. [score:7]
Thus, we cannot rule out the possibility that translational inhibition of other targets in the developing heart by miR-130a may also contribute to the phenotype we have observed in our miR-130a transgenic embryos. [score:7]
Overexpression of miR-130a inhibits translation of mRNA containing the 3′UTR of FOG-2.. [score:7]
When coupled to a reporter, the FOG-2 3′ UTR inhibits translation over 3-fold in a cell line expressing miR-130a. [score:7]
Taken together with the loss of function experiments described above, these results demonstrate that miR-130a targets the FOG-2 3′ UTR to inhibit mRNA translation. [score:7]
Our results are consistent with this notion, although do not rule out that miR-130a may also target other messages for degradation instead of translational inhibition as seen with the FOG-2 3′UTR. [score:7]
In addition to targeting FOG-2, miR-130a also likely targets other genes involved in heart development. [score:6]
The miR-130a target site in the FOG-2 3′UTR is required for translational repression. [score:5]
We also used a gain of function approach to demonstrate miR-130a's role in mediating translational repression of FOG-2. As a first step toward this end, we sought to identify a cell line that did not express miR-130a. [score:5]
As shown in figure 4E, the addition of miR-130a to COS-7 fibroblasts inhibited luciferase translation by 52±4% (p<0.0001). [score:5]
Cardiac overexpression of miR-130a results in decreased FOG-2 expression and a thin ventricular myocardial wall. [score:5]
An analysis of the miRNAs that are predicted to target the FOG-2 UTR demonstrated that miR-130a was the most highly expressed (Fig. 1A). [score:5]
The thin compact zone and ventricular septal defect are similar to those seen in FOG-2 deficient hearts, providing further support to the notion that miR-130a may play a role in the regulation of cardiac development through the modulation of FOG-2 translation. [score:5]
A direct demonstration of miR-130a's function during development must await the generation of mice with a targeted disruption of the miR-130a gene. [score:5]
Though several factors may contribute to the dynamic pattern of FOG-2 protein expression during development, these results are consistent with the notion that miR-130a may play a role in regulating FOG-2 protein levels. [score:5]
Since mice heterozygous for a disruption in the FOG-2 gene do not have any cardiac phenotype [18] and only express 50% of normal FOG-2 levels (G. K. and E. S., unpublished observations), it is likely that transgenic mice with low level miR-130a expression may also not develop cardiac malformations due to only modest reductions in FOG-2 protein levels. [score:5]
Thus, expression of miR-130a and FOG-2 overlaps in the heart and lung and suggests that in these tissues miR-130a might modulate translation of the FOG-2 message. [score:5]
As expected, the anti-miR-130a 2′-O-methyl oligonucleotide had no effect on the translational efficiency of the reporter with a mutation of the A site (compare columns 4 & 5, Fig. 3E). [score:4]
In this report, we have demonstrated that the 3′ UTR of FOG-2 contains an evolutionarily conserved region that regulates translational efficiency in a miR-130a -dependent fashion. [score:4]
These results support the hypothesis that translation of FOG-2 mRNA is regulated by miR-130a in cardiomyocytes in vivo. [score:4]
To study the effect of miRNA-130a on cardiac development, we generated transgenic mice with expression of the miR-130a precursor driven by the β-MHC promoter. [score:4]
To demonstrate the importance of the putative miR-130a binding site within the FOG-2 3′UTR for mediating translational repression, we generated a reporter construct with a mutation of the predicted binding site in the FOG-2 3′ UTR (Fig. 3A). [score:4]
In (E), COS-7 fibroblasts were transfected with a luciferase reporter containing the 3′ UTR of FOG-2 (columns 1 & 2) or the ΔA mutation (columns 3 & 4) in the absence (columns 1 & 3) or presence (columns 2 & 4) of the miR-130a expression construct. [score:4]
To examine expression of miR-130a in the developing heart, we took a PCR -based approach given the small amount of tissue available for RNA preparation at these early time points in development. [score:4]
MicroRNA-130a is expressed in the heart and is predicted to target a conserved region of the FOG-2 UTR. [score:4]
MicroRNA-130a acts through the conserved site in the FOG-2 UTR to mediate translational inhibition. [score:4]
In contrast, translational repression of the reporter construct was relieved in a dose -dependent fashion with the addition of increasing amounts of anti-miR-130a 2′-O-methyl oligonucleotide, resulting in luciferase levels that were equivalent to those seen with the mutated A site in the FOG-2 UTR (compare columns 3 & 4, Fig. 3E). [score:3]
An alignment of the FOG-2 3′ UTRs from human, mouse, rat, dog, cow, chicken, and zebrafish at the predicted miR-130a target site is shown in figure 1B. [score:3]
To demonstrate the effect of miR-130a overexpression on FOG-2 protein levels, we performed western analysis of βMHC-miR-130a transgenic hearts using an anti-FOG-2 antibody. [score:3]
This may be explained in part by approximately 25% of our F0 transgenic embryos not expressing significantly increased levels of miR-130a (Fig. 5A). [score:3]
Shown in (C) is a schematic of the miR-130a expression construct. [score:3]
Consistent with these results, we have shown that miR-130a is expressed in a tissue-restricted fashion, with highest levels in the heart and lung. [score:3]
Not surprisingly, addition of miR-130a did not significantly alter luciferase activity resulting from constructs with the altered target site (ΔA, columns 3 and 4, figure 4E). [score:3]
As a first step, we harvested transgenic embryos at embryonic day 13.5 and isolated total RNA to perform quantitative RT-PCR to confirm increased expression of miR-130a. [score:3]
‘*’ indicates a statistically significant difference (p<0.01 )To demonstrate that miR-130a is required to mediate translational repression via site A in the FOG-2 3′ UTR, we took two approaches. [score:3]
Finally, it is interesting that the miR-130a target site in the FOG-2 UTR is highly conserved in species from chicken to human, but is not conserved in the two zebrafish orthologues of FOG-2, fog2a and fog2b [40]. [score:3]
The transgenic miR-130a over -expression construct, pβ-MHC-miR-130a, was generated by inserting the miR-130a genomic fragment described above into a plasmid containing 5.6 kb of the murine β-MHC promoter and the human growth hormone polyadenylation signal [42]. [score:3]
Northern analysis has confirmed expression of miR-130a in mouse embryonic fibroblasts and both human and mouse ES cells as well as murine NIH 3T3 fibroblasts and mouse lung [25], [35], [36]. [score:3]
Due to the lethality of FOG-2 deficient mice at embryonic day 13.5, we suspected that transgenic over -expression of miR-130a might also lead to embryonic lethality and thus we would be unable to establish a viable transgenic line. [score:3]
Overexpression of microRNA-130a in embryonic cardiomyocytes results in structural heart defects. [score:3]
As can be seen in Figure 4B, the wild-type and ΔA constructs produced no significant difference in luciferase activity, consistent with the notion that miR-130a acts through the A site and that in the absence of miR-130a, deletion of this site has no effect on the ability of the UTR to modulate translational efficiency. [score:3]
These observations strongly suggest that miR-130a is acting through the A site of the FOG-2 3′UTR to mediate translational repression. [score:3]
This result demonstrates that miR-130a is present in the embryonic heart and regulated in a dynamic pattern throughout heart development. [score:3]
In (A), expression of miR-130a as determined by quantitative RT-PCR on four wild type (WT) and four transgenic hearts (TG-1 thru 4) at embryonic day 13.5. represent the mean±S. [score:3]
In (D), northern analysis using a probe specific for miR-130a and 20 µg total RNA from COS-7 fibroblasts transfected with increasing amounts of the miR-130a expression construct shown in (C). [score:3]
In (B), an alignment of the predicted miR-130a target site in the FOG-2 3′ UTR from several different species as predicted by MicroRNA. [score:3]
The 3.3-fold miR-130a -dependent translational repression seen on the FOG-2 3′ UTR (Fig. 3) is comparable to what has been reported for other vertebrate UTRs examined to date [11], [31], [32], [33]. [score:3]
In addition, another 25% of our transgenic embryos expressed levels of miR-130a that were sufficient to only decrease FOG-2 protein levels by less than 50%. [score:3]
In the miR-130a transgenic embryos, FOG-2 levels should only be reduced in cardiomyocytes, since the β-MHC promoter used to drive expression of miR-130a in our transgenic mice is not active in the developing endocardial cushions or epicardium [30]. [score:3]
Upon expression, this precursor is recognized and processed by the miRNA processing enzymes Drosha and Dicer to produce mature miR-130a. [score:3]
Further, the 2 live born transgenic pups were found not to express increased levels of miR-130a in their hearts (data not shown), suggesting that these animals survived because the transgene had been silenced in these animals, perhaps due to integration site effects. [score:3]
We then transfected these constructs into NIH 3T3 fibroblasts, since it had been previously shown that this cell line expresses miR-130a [25]. [score:3]
Pronuclear injections were performed into CD-1 or C57BL/6 oocytes using a 10 kb fragment of pβ-MHC-miR-130a containing 5.6 kb of the β-MHC promoter driving expression of miR-130a. [score:3]
As shown in figure 4D, this vector programmed expression of miR-130a in COS-7 cells in a dose -dependent fashion. [score:3]
To confirm that miR-130a was indeed expressed in the heart, we performed northern analysis on total RNA from several different adult mouse tissues using a radiolabeled probe specific to miR-130a (Fig. 1C). [score:3]
‘*’ indicates a statistically significant difference (p<0.01 ) To demonstrate that miR-130a is required to mediate translational repression via site A in the FOG-2 3′ UTR, we took two approaches. [score:3]
0006161.g005 Figure 5 In (A), expression of miR-130a as determined by quantitative RT-PCR on four wild type (WT) and four transgenic hearts (TG-1 thru 4) at embryonic day 13.5. represent the mean±S. [score:3]
Using northern analysis, we found that the COS-7 monkey kidney fibroblast cell line does not express detectable levels of miR-130a (Fig. 4A). [score:3]
As can be seen, miR-130a is predominately expressed in the heart and lung, with lower amounts in the kidney. [score:3]
Of note, one of the four transgenic embryos examined did not express significantly higher levels of miR-130a, consistent with our observation of live born transgenic pups as described above. [score:3]
The miR-130a expression construct was generated using PCR to amplify a 467 bp fragment encoding the miR-130a precursor from mouse genomic DNA with the primers 5′CACTCGAGCTCTGGACAGGTCTACAAAAATGGand 5′-CATTGCGGCCGCCCTTGAGAAGTGTCAAATGATGG. [score:2]
We found that compared to wild type littermates, 75% of βMHC-miR-130a transgenic embryos displayed a significant increase in miR-130a expression (Fig. 5A). [score:2]
Therefore, we chose instead to analyze our miR-130a transgenics as F0 lines between embryonic days 13.5 to 14.5 of development. [score:2]
Quantitative RT-PCR performed with RNA prepared from hearts at embryonic day 11.5, 13.5, 15.5, neonatal (P0), and adult revealed the highest levels of miR-130a expression at birth with levels approximately 3-fold greater compared to the adult heart (compare columns 4 & 5, Fig. 1D). [score:2]
This generated a FOG-2 UTR with a 20 bp mutation in the predicted miR-130a binding site. [score:2]
MicroRNA-130a is expressed in the heart. [score:2]
COS-7 and NIH 3T3 fibroblasts were transfected using Superfect (Qiagen, Valencia, CA) with 200 ng pVRβGal, 2 µg luciferase reporter plasmid, 0–2 µg of the anti-miR-130a 2′-O-methyl oligonucleotide (5′-GCCCUUUUAACAUUGCACUC) and pcDNA3 to a total of 5 µg DNA as described previously [44]. [score:1]
Subsequently it was hybridized with 20 ng/ml of a [32]P-radiolabeled LNA oligonucleotide complementary to miR-130a(5′-GCCCTTTTAACATTGCACTC) in Hyb buffer at 35°C overnight. [score:1]
This suggests that miR-130a may have a distinct function in higher vertebrates during heart development as compared with its function in zebrafish. [score:1]
Thus, it is not surprising that the miR-130a transgenic embryos do not fully recapitulate the phenotype of the FOG-2 [−/−] embryos. [score:1]
For northern analysis of miR-130a, 100 µg of total RNA was resolved by 15% denaturing polyacrylamide gel electrophoresis and then transferred to a Hybond N+ membrane using a semidry transfer apparatus (Bio-Rad, Hercules, CA) at 300 mA for 90 mins. [score:1]
‘*’ indicates a statistically significant difference (p<0.01 ) In (A), northern analysis using 20 µg total RNA from COS-7 or NIH 3T3 cell lines with a probe specific for miR-130a. [score:1]
However, the thin compact zone seen in the miR-130a transgenic mice is similar to that seen in the FOG-2 deficient mice, suggesting that this phenotype may be due to reduced FOG-2 levels. [score:1]
In (D - G), transverse sections of embryonic day 14.5 hearts from wild type (D, F) and β-MHC-miR-130a transgenics (E, G) stained with hematoxylin and eosin. [score:1]
In this report, we describe the identification and characterization of an evolutionary conserved target site in the 3′ UTR of FOG-2 for microRNA-130a (miR-130a). [score:1]
The ventricular septal defect seen in the miR-130a transgenics may be due to the failure of the myocardium in the proximity of the developing endocardial cushions to send the appropriate signals to allow for the normal maturation of the membraneous interventricular septum. [score:1]
Interestingly, as miR-130a levels peak in the neonate, FOG-2 protein levels decline (Fig. 1F). [score:1]
Shaded boxes indicate bases pairing with miR-130a. [score:1]
We designed a 2′-O-methyl oligonucleotide to specifically block miR-130a and co -transfected it along with our FOG-2 3′ UTR reporter constructs into 3T3 fibroblasts. [score:1]
0006161.g004 Figure 4 In (A), northern analysis using 20 µg total RNA from COS-7 or NIH 3T3 cell lines with a probe specific for miR-130a. [score:1]
In (C), northern analysis of 100 µg total RNA from different adult mouse tissues using a probe specific for miR-130a. [score:1]
In (F), graph of relative levels of miR-130a compared to FOG-2 protein levels during cardiac development. [score:1]
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[+] score: 305
Because miRNAs may inhibit target gene expression by blocking protein translation or by degrading mRNA, we evaluated whether miR-142-5p or miR-130a-3p influences the mRNA and protein expression of their target genes. [score:11]
Of the most significantly differentially expressed genes in M(IL-4) when transduced with miR-142-5p ASO or miR-130a-3p mimics, two master regulators of M2 polarization 2, SOCS1 expression was elevated and PPARγ expression was reduced (Fig. 4a), suggesting that these genes are potential targets of miR-142-5p and miR-130a-3p, respectively. [score:10]
Therefore, miR-142-5p upregulation and miR-130a-3p downregulation in M2 macrophages help to maintain M2 signalling by altering SOCS1 and PPARγ expression. [score:9]
Because the activator of M1 macrophages, LPS, enhances the nuclear translocation of Sp1, leading to overexpression of its target genes 24, we speculated that IL-4 might inhibit Sp1 signalling and subsequently repress miR-130a expression in M2 macrophages. [score:9]
MiRanda and TargetScan predicted SOCS1 as the target gene of miR-142-5p, while all three miRNA target prediction databases predicted PPARγ as the target gene of miR-130-3p. [score:9]
Treatment with STAT6 inhibitors or transduction with STAT6-shRNA in M(IL-4) dramatically reduced HDAC2 expression (Fig. 8l), reversed histone deacetylation at the miR-130a promoter and rescued miR-130a-3p expression (Fig. 8m). [score:7]
Collectively, our data suggested that miR-142-5p downregulation and miR-130a-3p upregulation synergistically enhance the profibrogenic activities of macrophages. [score:7]
These findings may have clinical applications, as miR-142-5p is upregulated and miR-130a-3p is downregulated in the macrophages in livers of patients with liver cirrhosis and in those in the BAL fluid of IPF patients. [score:7]
To identify the target genes of miR-142-5p and miR-130a-3p that are involved in M2 polarization, we examined the mRNA expression profile changes after altering miR-142-5p or miR-130a-3p expression in M(IL-4). [score:7]
Our study showed that miR-130a-3p targets PPARγ, while Th2 stimulation suppresses miR-130a-3p expression by inducing histone deacetylation at its promoter region, thus relieving its repression of PPARγ. [score:7]
Transduction of macrophages with either miR-142-5p ASO or miR-130a-3p mimics significantly reduced the expression of M2 markers (Fig. 2b–d and Supplementary Fig. 2c,d) and pinocytosis (Supplementary Fig. 2e) induced by IL-4. Of note, upregulation of the M2 markers and pinocytosis induced by IL-4 was almost completely abrogated when both miR-142-5p ASO and miR-130a-3p mimics were transduced. [score:6]
Knockdown or forced expression of miR-142-5p or miR-130a-3p in fibroblasts had no appreciable effects of TGF-β1 expression or activation (Supplementary Fig. 3f). [score:6]
miR-142-5p expression was significantly increased in the macrophages of the cirrhotic liver tissues compared with normal liver tissues resected from patients with hepatic haemangioma, while miR-130a-3p expression was markedly decreased (Fig. 9i), demonstrating the correlation of altered miR-142-5p and miR-130a-3p expression in hepatic macrophages of liver cirrhosis. [score:6]
Consistent with our findings in human macrophages, IL-4 increased miR-142-5p expression and reduced miR-130a-3p expression in mouse macrophages (Fig. 6b). [score:5]
In contrast, IL-4 reduced miR-130a-3p expression at 8 h, this expression fell to the lowest point by 24 h and remained at a low level for 48 h (Fig. 4h). [score:5]
Furthermore, silencing HDAC2 in M(IL-4) increased histone acetylation at the miR-130 promoter and miR-130a-3p expression (Fig. 8j,k), suggesting that IL-4 induces histone deacetylation of the miR-130a promoter by enhancing HDAC2 expression. [score:5]
Additionally, TGF-β1 expression and activation in the co-cultured fibroblasts were suppressed by miR-142-5p and miR-130a-3p (Fig. 3g). [score:5]
Consistent with our findings in mouse lung fibrosis, miR-142-5p expression in the macrophages of BAL fluid from IPF patients was increased, while miR-130a-3p expression was reduced (Fig. 10g). [score:5]
PPARγ elevation in M(IL4) was inhibited by rescuing miR-130-3p expression with miRNA mimics, but was retrieved by co-transfection with PPARγ-mut carrying a mutated miR-130-3p seed sequence at its 3′ UTR, but not with a wild-type PPARγ vector (Fig. 5d). [score:5]
Next, we investigated the mechanisms by which IL-4 upregulates miR-142-5p but downregulates miR-130a-3p. [score:5]
Corn oil gavage with carbon tetrachloride (CCL [4]) in mice resulted in massive liver fibrosis (Fig. 9a,f) as reported previously 25, and led to increased miR-142-5p expression and decreased miR-130a-3p expression in the isolated hepatic macrophages (Fig. 9b). [score:5]
Furthermore, inhibiting miR-130a-3p expression in resting macrophages with ASO enhanced PPARγ mRNA and protein levels, while miR-130a-3p mimics reduced PPARγ mRNA and protein levels in M(IL-4) (Fig. 4e,f). [score:5]
We further determined whether elevated PPARγ expression due to reduced miR-130-3p expression contributes to M2 polarization in M(IL4). [score:5]
We identified few CpG islands at the promoter of miR-130a (Supplementary Fig. 5d), and treatment with 5-Aza-dC, a DNA methyltransferase inhibitor, failed to restore miR-130a expression in IL-4 -treated macrophages (Supplementary Fig. 5e), excluding the contribution of DNA methylation to reduced miR-130a in M2 macrophages. [score:5]
More importantly, inhibiting miR-142-5p and increasing miR-130a-3p expression with LNA -modified oligonucleotides alleviated both CCL [4] -induced liver fibrosis and bleomycin -induced lung fibrosis, highlighting the therapeutic importance of these miRNAs. [score:5]
Collectively, modulating the expression of miR-142-5p and miR-130a-3p in hepatic macrophages inhibits the progression of liver fibrosis. [score:5]
TSA, an inhibitor of class I and II HDACs, relieved the IL-4 -mediated inhibition of miR-130a transcription (Fig. 8f), suggesting that histone deacetylation is responsible for reduced accessibility of Sp1 to the promoter region of miR-130a. [score:5]
miR-142-5p and miR-130a-3p regulate profibrogenesis by targeting SOCS1 and PPARγ respectively. [score:4]
Taken together, these results indicated that aberrant miR-142-5p and miR-130a-3p expression in lung macrophages might be involved in the development of pulmonary fibrosis. [score:4]
To investigate whether miR-142-5p and miR-130a-3p could directly mediate the TGF-β1 expression in fibroblasts, we examined their expression levels of these miRNAs in fibroblasts. [score:4]
IL-4 downregulates miR-130a-3p by inducing histone deacetylation. [score:4]
IL-4 downregulates miR-130a-3p by histone deacetylation. [score:4]
Moreover, inhibitors of Sp1 (Supplementary Fig. 5b) efficiently abrogated the luciferase activities of the miR-130a promoter. [score:3]
Therefore, our findings suggested the therapeutic potential of inhibiting miR-142-5p and elevating miR-130a-3p in macrophages to treat lung fibrosis. [score:3]
Therefore, SOCS1 and PPARγ are target genes of miR-142-5p and miR-130a-3p, respectively. [score:3]
Furthermore, combined treatment with both miR-142-5p ASO and miR-130a-3p mimics almost completely abrogated profibrotic marker expression in hepatic macrophages and liver fibrosis (Fig. 9a–f). [score:3]
Aligned with the kinetics of miR-130a-3p reduction, PPARγ expression increased by 8 h and was maintained at a high level for 48 h (Fig. 4h). [score:3]
More importantly, treatment with miR-142-5p ASO elevated SOCS1 levels and reduced STAT6 phosphorylation, while treatment with miR-130a-3p mimics repressed PPARγ expression (Fig. 9c). [score:3]
Indeed, administration of miR-142-5p ASO or/and miR-130a-3p mimics successfully prevented fibrosis in two major fibrotic disease mouse mo dels. [score:3]
To determine the clinical relevance of our findings, we examined the expression of miR-142-5p and miR-130a-3p using fluorescence in situ hybridization (FISH) in the liver samples of patients with hepatitis B induced liver cirrhosis. [score:3]
After 24 h, the cells were stimulated with IL-4 for 24 h and expression of miR-142-5p and miR-130a-3p was examined by (mean±s. [score:3]
Transduction of miR-142-5p ASO and miR-130a-3p mimics in IL-4 -treated mouse macrophages synergistically inhibited M2 polarization (Fig. 6c,d) and their profibrogenic effect (Fig. 6e,f). [score:3]
To determine whether miR-142-5p and miR-130a-3p are involved in human IPF, we isolated macrophages from the bronchial alveolar lavage (BAL) fluid of normal volunteers and IPF patients and examined the expression of miR-142-5p and miR-130a-3p by. [score:3]
Importantly, administration of LNA -modified miR-142-5p ASO and miR-130a-3p mimic failed to inhibit CCL [4] -induced liver fibrosis in Ccr2 [−/−] mice (Supplementary Fig. 6a). [score:3]
Furthermore, transducing the M(IL-4) with miR-142-5p ASO and miR-130a-3p mimics synergistically inhibited their ability to stimulate collagen production and proliferation of fibroblasts when co-cultured (Fig. 3d–f and Supplementary Table 2). [score:3]
Transduction of M(IL-4) with miR-142-5p ASO and miR-130a-3p mimics abrogated the ability of macrophages to induce FAP and α-SMA expression in the fibroblasts (Fig. 3b,d). [score:3]
Collectively, miR-130a-3p transcription in resting macrophages is maintained by Sp1 but is inhibited in M(IL-4) by histone deacetylation at its promoter, which is mediated by STAT6 -induced HDAC2. [score:3]
Moreover, recovering PPARγ expression in M(IL-4) that were transfected with miR-130-3p mimics retrieved M2 polarization (Fig. 5e) and the profibrogenic effects of the macrophages (Fig. 5f). [score:3]
However, intravenous injection of LNA -modified miR-142-5p ASO or miR-130a-3p mimics following CCL [4] challenge reduced miR-142-5p and increased miR-130a-3p in the hepatic macrophages to normal ranges (Fig. 9b), consistent with previous findings that LNA -modified oligonucleotides alter miRNA expression in immune cells in vivo 27 28. [score:3]
We used locked nucleic acid (LNA) -modified miR-142-5p ASO or/and miR-130a-3p mimic that are more stable in vivo and with less off-target effects 27 28. [score:3]
miR-142-5p and miR-130a-3p target the 3′UTRs of SOCS1 and PPAR γ respectively. [score:3]
miR-130a expression was determined by 24 h afterwards (n=3). [score:3]
Because miRNAs may participate in signal transduction feedback circuits by maintaining the expression of signalling proteins 23, we further evaluated the contributions of miR-142-5p and miR-130a-3p in maintaining SOCS1 and PPARγ levels in M2 macrophages by examining the kinetics of the miRNAs and their target genes in macrophages following IL-4 treatment. [score:3]
Mechanistically, the elevated miR-142-5p prolongs STAT6 phosphorylation by targeting SOCS1, while miR-130a reduction relieves its repression of PPARγ, a STAT6 coordinator. [score:3]
Dyregulated Mϕ miR-142-5p and miR-130a-3p enhance lung fibrosis. [score:2]
miR-142-5p and miR-130a-3p regulate M2 activation of macrophages. [score:2]
miR-142-5p and miR-130a-3p regulate the profibrogenesis of macrophages. [score:2]
Dyregulated Mϕ miR-142-5p and miR-130a-3p enhance liver fibrosis. [score:2]
How to cite this article: Su, S. et al. miR-142-5p and miR-130a-3p are regulated by IL-4 and IL-13 and control profibrogenic macrophage program. [score:2]
Nevertheless, our data and those of another group 43 indicated that miR-142-5p and miR-130a-3p were dysregulated in multiple organ fibrosis of both humans and mice. [score:2]
miR-142-5p and miR-130a-3p regulate profibrogenesis of mouse macrophages. [score:2]
Next, we further evaluated whether aberrant HDAC expression is responsible for histone deacetylation of miR-130a promoter in M(IL-4). [score:1]
To further confirm the roles of miR-142-5p and miR-130a-3p in M2 polarization, we transduced M(IL-4) with miR-142-5p ASO or/and miR-130a-3p mimics and adjusted their miRNA levels to those in the untreated cells (Supplementary Fig. 2b). [score:1]
PPARγ complementary DNA carrying a wide-type 3′UTR or 3′UTR with a mutated seed sequence for miR-130a-3p (PPARγ-mut1) were cloned into pcDNA 3.1 for rescue experiments 58. [score:1]
For LNA -modified oligonucleotides treatment, intravenous injection of LNA -modified miR-142-5p ASO, miR-130a-3p mimics, scramble control ASO or scramble control mimics (Exiqon) was performed 24 h after the initiation of CCL [4] or 16 days after bleomycin challenge at a dose of 0.15 mg g [−1] body weight and was repeated every 3 days thereafter. [score:1]
Similarly, using a series of pGL3 reporter plasmids containing various deleted (Supplementary Fig. 5a) or mutated (Supplementary Fig. 5b) 5'-flanking regions of miR-130a, we identified a Sp1 -binding site for miR-130a (Fig. 8a). [score:1]
The seed sequence of miR-142-5p at SOCS1-3′ UTR and that of miR-130a-3p at PPARγ-3′ UTR are conserved among humans and mice (Fig. 6a). [score:1]
A series of nested deletions were generated using miR-142 (−1911/+91)-luc or miR-130a (−1891/+91)-luc as the template and the forward primers listed in Supplementary Table 3. The point mutations were introduced into the by QuikChange Site-Directed Mutagenesis Kit (Stratagene) using primers listed in Supplementary Table 3 according to manufacturer's instructions. [score:1]
Cells were transfected with 10 pmol miR-142-5p mimics, miR-130a-3p mimics or scramble controls (Qiagen) and co -transfected with 0.2 μg per well wild-type SOCS1 3′ UTR-luc, mutant SOCS1 3′ UTR-luc, wild-type PPARγ 3′ UTR-luc or mutant PPARγ 3′ UTR-luc, respectively, using JetPEI transfection reagent (Polyplus transfection, Illkirch, France) according to the manufacturer's instructions. [score:1]
The wild-type or mutant 3′ UTRs of SOCS1 and PPARγ containing the predicted miR-142-5p or miR-130a-3p binding sites were synthesized (GeneArt, Lifetechnologies, Germany) and cloned into the pGL3.0-control vectors according to the manufacturer's instructions (Promega, Madison, WI). [score:1]
Additionally, co-culturing the fibroblasts with M(IL-4) enhanced the ability of the fibroblasts to contract collagen gel; this enhancement was substantially attenuated when miR-142-5p was reduced or/and miR-130a-3p was increased in the co-cultured macrophages (Fig. 3c). [score:1]
We observed that transduction of the macrophages with miR-142-5p ASO or miR-130a-3p mimics, but not with other oligonucleotides, reduced CCL18 secretion following IL-4/IL-13 treatments (Supplementary Fig. 2a). [score:1]
In contrast, LNA -modified miR-142-5p ASO and miR-130a-3p mimic did not exert anti-fibrotic effects against bleomycin -induced lung lesion in Ccr2 [−/−] mice (Supplementary Fig. 6b). [score:1]
The in vivo functions of macrophage-related miR-142-5p and miR-130a-3p were also studied in wild-type and Ccr2 [−/−] mouse mo dels of lung fibrosis induced by bleomycin 31 32. [score:1]
Collectively, our data suggested that miR-142-5p and miR-130a-3p synergistically control M2 macrophage polarization. [score:1]
Then, the sections were hybridized with 20 nM 5' digoxigenin -labelled LNA control probe and miR-142-5p or miR-130-3p probe (Exiqon) overnight at 42 °C, then rinsed twice with 5 × SSC at room temperature, washed three times in 2 × SSC/50% formamide at hybridization temperature for 20 min and washed four times in PBS with 0.1% Tween 20 (PBST). [score:1]
Indeed, the therapeutic effects of LNA -modified miR-142-5p ASO and miR-130a-3p mimics against fibrosis were absent in Ccr2 [−/−] mice. [score:1]
Here, we demonstrated that increased miR-142-5p and reduced miR-130a-3p in macrophages upon Th2 stimulation help to maintain M2 polarization and their profibrogenic activities. [score:1]
Thus, miR-142-5p and miR-130a-3p reduce the mRNA stability of SOCS1 and PPARγ mRNA in macrophages, respectively. [score:1]
Furthermore, ChIP analysis using RNA pol II antibody demonstrated that IL-4-reduced chromatin accessibility at the miR-130a promoter (Fig. 8d). [score:1]
Co-transfection with miR-142-5p mimics specifically reduced the luciferase activity of the SOCS1-3′ UTR transfected cells, while miR-130a-3p mimics reduced that of the PPARγ-3′ UTR transfected cells (Fig. 4b). [score:1]
To further explore the therapeutic potentials of LNA -modified oligonucleotides in lung fibrosis, we administered bleomycin intratracheally into wild-type mice and initiated intravenous injection of LNA -modified miR-142-5p ASO or/and miR-130a-3p mimic 16 days after bleomycin challenge, which was then repeated every 3 days until 28d, when the animals were sacrificed for examination. [score:1]
To determine whether the effects of blocking miR-142-5p and supplementing miR-130a-3p are synergistic, we employed a combination index (CI) to indicate synergistic (CI<1), additive (CI=1) and antagonistic (CI>1) effects of miR-142-5p ASO and miR-130a-3p mimics on M2 cytokine production, respectively. [score:1]
Moreover, our findings that blocking miR-142-5p with ASO together with increasing miR-130a-3p with miRNA mimics almost completely abrogated M2 activation and their profibrogenic effects support the finding that changes in the levels of multiple miRNAs may act synergistically to sustain macrophages in a certain activation status. [score:1]
Collectively, our data suggest that miR-142-5p and miR-130a-3p mediate M2 polarization and profibrogenic effects in both humans and mice. [score:1]
IL-4/IL-13 increases miR-142-5p via STAT6 and reduces miR-130a-3p by histone deacetylation in macrophages. [score:1]
Interestingly, although IL-4 reduced Sp1 binding to the miR-130a promoter (Fig. 8b), nuclear translocation of the transcription factor remained unchanged upon IL-4 treatment (Fig. 8c and Supplementary Fig. 5c). [score:1]
Briefly, 1 × 10 [6] cells were transfected with 200 pmol mouse miR-142-5p ASO or the scramble negative control and 10 pmol mouse miR-130a-3p or scramble negative control (Qiagen). [score:1]
Similar to the findings in liver fibrosis, administering miR-142-5p ASO and miR-130a-3p mimics significantly reduced the degree of lung fibrosis in the bleomycin -treated mice (Fig. 10c,d). [score:1]
DNA probes containing the STAT6 site of the miR-142 promoter or the SP1 site of the miR-130a promoter (Supplementary Table 3) were labelled at the 3'-end with biotin using a Biotin 3'End DNA Labelling Kit (Pierce), according to the manufacturer's instructions. [score:1]
Similar to their effects on hepatic fibrogenesis, the transduction of miR-130a-3p mimics and miR-142-5p ASO to M(IL-13) synergistically abrogated the profibrotic effects of these cells in the lungs (Fig. 10b). [score:1]
Quantification of miR-142-5p [+] and miR-130a-3p [+]macrophages (normal liver group, n=24; cirrhotic liver group, n=39, mean±s. [score:1]
These fragments were fused to pGL3-Basic vector (5'KpnI and 3' XhoI, Promega) to generate miR-142 (−1911/+91)-luc and miR-130a (−1891/+91)-luc, respectively. [score:1]
To study the particular roles of miR-142-5p and miR-130a-3p in profibrotic macrophages in vivo, we transduced miR-142-5p ASO or/and miR-130a-3p mimics to wild-type M(IL-13) and transferred these cells to Ccr2 [−/−] mice challenged with bleomycin. [score:1]
Next, we examined histone modifications on the miR-130a-3p promoter by ChIP using AcH4 and H3K4me3 as markers of open chromatin and H3K9me3 and H3K27me3 as markers of closed chromatin. [score:1]
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[+] score: 274
The TNF-α 3′UTR containing the mutated ssc-miR-130a-3p target sequence (TTGCACT to AACGTGA), ssc-miR-181a target sequence (TGAATGT to ACTTACA), ssc-miR-181b target sequence (TGAATGT to ACTTACA), ssc-miR-301a-3p target sequence (TTGCACT to AACGTGA), mmu-miR-130a-3p target sequence (TTGCACT to AACGTGA), mmu-miR-181a target sequence (TGAATGT to ACTTACA), mmu-miR-181b target sequence (TGAATGT to ACTTACA), mmu-miR-301a-3p target sequence (TTGCACT to AACGTGA), and mmu-miR-351-5p target sequence (CTCAGGG to GAGTCCC) were cloned into the pMIR-REPORT Luciferase vector. [score:19]
Herein, we further identified miR-181a and miR-301a-3p to be involved in the posttranscriptional regulation of TNF-α in both Omp25-expressed PAMs and mouse RAW264.7 cells, yet found that Omp25 specially induced miR-130a-3p to inhibit TNF-α expression in porcine macrophages, and Omp25 specially induced miR-351-5p to inhibit TNF-α expression in murine macrophages via targeting the 3′UTR of TNF-α. [score:14]
Downregulation of Omp25-Induced miRNAs Improves TNF-α Production and Promotes Intracellular Bacterial Clearance in WT B. suis-Infected MacrophagesNow we have shown that Omp25 expression can induce miR-130a-3p, miR-146a, miR-181a, miR-301a-3p, or miR-351-5p in PAMs and mouse RAW264.7 cells, but whether or not the WT B. suis infection can also upregulate the expression of these miRNAs needs to be examined. [score:11]
These data demonstrate miR-130a-3p, miR-181a, miR-181b, or miR-301a-3p regulates the TNF-α expression at the transcriptional level via targeting its 3′UTR, while miR-351-5p may inhibit murine TNF-α expression both at transcriptional and posttranscriptional level. [score:10]
Taken together, the results present in here demonstrate that miR-130a-3p, miR-181a, and miR-301a-3p regulate TNF-α expression at posttranscriptional level, miR-146a regulates TNF-α expression at posttranscriptional level, whereas miR-351-5p specifically regulate mouse TNF-α expression at both transcriptional and posttranscriptional levels. [score:10]
Although miR-130a-3p can target the 3′UTR of TNF-α derived from different mammals, miR-130a-3p inhibitor only could attenuate the inhibitory effect of Omp25 in PAMs since miR-130a-3p was only induced in Omp25-expressed PAMs, but not in RAW264.7 cells. [score:9]
These results suggest that miR-130a-3p, miR-181a, miR-181b, and miR-301a-3p inhibit TNF-α expression at the posttranscriptional level, while miR-146a and miR-351-5p likely inhibit TNF-α expression in transcriptional level. [score:9]
In this study, we found that the inhibition of miR-130a-3p, -181a, and -301a-3p partially blocked Om25 -induced TNF-α inhibition, while inhibition of miR-146a or miR-351-5p attenuates the inhibitory effects of Omp25 or WT B. suis on TNF-α transcription. [score:9]
Further studies revealed that miR-130a-3p, miR-181a, and miR-301a-3p target to the 3′UTR region of TNF-α to restrain TNF-α production at the posttranscriptional level, whereas miR-146a and miR-351-5p transcriptionally suppress the expression of TNF-α by targeting TRAF6 and IRAK1 (Figure 9). [score:9]
Our results showed that in Omp25 -expressing PAMs, the levels of miR-130a-3p, miR-146a, miR-181a, miR-181b, and miR-301a-3p were upregulated, while miR-125a-5p, miR-125b-5p, and miR-146b were downregulated compared to controls (Figure 4A). [score:8]
Now we have shown that Omp25 expression can induce miR-130a-3p, miR-146a, miR-181a, miR-301a-3p, or miR-351-5p in PAMs and mouse RAW264.7 cells, but whether or not the WT B. suis infection can also upregulate the expression of these miRNAs needs to be examined. [score:8]
miR-130a has been reported to downregulate the expression of TNF-α, thereby inhibiting the activation of macrophage (26, 43). [score:8]
To further determine the roles of miR-130a-3p, miR-146a, miR-181a, miR-181b, miR-301a-3p, and miR-351-5p in regulating TNF-α, cells were transfected with inhibitor control, miR-130a-3p, miR-146a, miR-181a, miR-181b, miR-301a-3p, miR-351-5p inhibitor, or miRNA inhibitor mix and infected with LV-Omp25 or LV-Blank. [score:8]
In PAMs, transfection of miR-130a-3p, miR-146a, miR-181a, and miR-301a-3p inhibitors apparently improved the relative TNF-α levels compared with the inhibitor control, but miR-181b and miR-351-5p inhibitors had no effects on TNF-α expression (Figure 7A). [score:8]
These results not only further confirm that the inhibitory effect of miR-130a-3p, miR-181a, or miR-301a-3p on TNF-α is at posttranscriptional level, likely by targeting to the 3′UTR of TNF-α, but also demonstrate that Brucella Omp25 regulates TNF-α expression by multiple modes of action. [score:8]
Notably, in PAMs transfected with a mix of miR-130a-3p, miR-146a, miR-181a, and miR-301a-3p inhibitors, as well as in mouse RAW264.7 cells transfected with a mix of miR-146a, miR-181a, miR-301a-3p, and miR-351-5p inhibitors, the inhibitory effects of Omp25 on TNF-α induction were further attenuated, leading to the levels of TNF-α were almost close to that of LV-Blank (Figures 7A,B). [score:7]
Omp25 Upregulates miR-146a, -181a, -181b, and -301a-3p in Both PAMs and Mouse RAW264.7 Cells, but Separately Upregulates miR-130a-3p and miR-351-5p in These Two Cells. [score:7]
Figure 8Deficiency of Omp25 decreases B. suis -induced miR-130a-3p, miR-146a, miR-181a, miR-301a-3p, or miR-351-5p whereas inhibition of these miRNAs upregulates tumor necrosis factor (TNF)-α and promotes the intracellular clearance of wild-type (WT). [score:6]
In this study, we found that B. suis Omp25 upregulated miR-130a-3p, miR-146a, miR-181a, miR-301a-3p, or miR-351-5p, which was correlated with TNF-α inhibition. [score:6]
Importantly, B. suis infection induces higher levels expression of miR-146a, miR-181a, miR-181b, or miR-301a-3p in both PAMs and mouse RAW264.7 cells, yet specifically upregulates miR-130a-3p in PAMs and miR-351-5p in RAW264.7 cells, respectively. [score:6]
At the posttranscriptional levels, Brucella Omp25 inhibits LPS -induced TNF-α via upregulating miR-181a and miR-301a-3p (in both porcine and murine macrophages), or miR-130a-3p (in porcine macrophages), or miR-351-5p (in murine macrophages). [score:6]
Since the synergistic regulation of these Omp25 -induced miRNAs in TNF-α production, simultaneous depletion of miR-130a-3p, -146a, -181a, and -301a-3p could almost completely block the inhibitory effects of Omp25 on LPS -induced TNF-α in PAMs infected with WT B. suis, and simultaneous depletion of miR-146a, -181a, -301a-3p, and -351-5p in mouse RAW264.7 cells could almost completely block Omp25 inhibition, thus promoting LPS -induced TNF-α and increasing intracellular clearance of Brucella in both cells. [score:6]
Altogether, these data demonstrate that Omp25 induces the expression of several miRNAs in PAMs and mouse RAW264.7 cells, with miR-146a, miR-181a, miR-181b, and miR-301a-3p being commonly upregulated in both PAMs and mouse RAW264.7 cells compared to miR-130a-3p and miR-351-5p, which are specific for PAMs and mouse RAW264.7 cells, respectively. [score:5]
In summary, the present data in this study provide certain evidences for miRNAs (miR-130a-3p, miR-146a, miR-181a, miR-301a-3p, and miR-351-5p) participation of Brucella Omp25 -induced TNF-α suppression in porcine and murine macrophages and demonstrate that different regulation patterns are employed by Omp25 between porcine and murine macrophages in this regulatory process. [score:5]
Figure 7miR-146a, miR-181a, and miR-301a-3p participate in the regulation of tumor necrosis factor (TNF)-α in both porcine alveolar macrophages (PAMs) and mouse RAW264.7 cells, whereas miR-130a-3p and miR-351-5p differentially regulate TNF-α expression in porcine and murine cells. [score:5]
miR-146a, miR-181a, and miR-301a-3p Participate in the Regulation of TNF-α in Both PAMs and Mouse RAW264.7 Cells, whereas miR-130a-3p and miR-351-5p Specially Regulates TNF-α Expression in Porcine and Murine Cells. [score:5]
In mouse RAW264.7 cells, except for miR-130a-3p and miR-181b inhibitors, other miRNA inhibitors significantly raised the relative levels of TNF-α (Figure 7B). [score:5]
miR-130a-3p, miR-146a, miR-181a, miR-181b, miR-301a-3p, and miR-351-5p Inhibit TNF-α Expression at Transcriptional or Posttranscriptional Levels. [score:5]
Altogether, these results indicate that miR-146a, miR-181a, and miR-301a-3p participate in the regulation of TNF-α in both PAMs and mouse RAW264.7 cells, whereas miR-130a-3p and miR-351-5p specifically regulate TNF-α expression in porcine and murine cells, respectively. [score:5]
These results demonstrate that in the process of Omp25 inhibiting TNF-α expression, miRNAs (miR-130a-3p, miR-146a, miR-181a, and miR-301a-3p) play principal roles in PAMs, while miRNAs (miR-146a, miR-181a, miR-301a-3p, and miR-351-5p) play principal roles in mouse RAW264.7 cells. [score:5]
We found that Omp25 -induced miR-146a, miR-181a, and miR-301a-3p regulate TNF-α in both PAMs and mouse RAW264.7 cells, whereas Omp25 -induced miR-130a-3p and miR-351-5p specifically regulate TNF-α expression in porcine and murine macrophages, respectively. [score:5]
The low homology of miR-130a putative promoter sequences between porcine and murine may cause significant difference in miR-130a expression in Omp25-expressed PAMs and RAW264.7 cells. [score:5]
As members of miR-130/301 family, miR-130a and miR-301a have been shown to be modulated by distinct transcriptional events (42) and are highly conserved for the 3′UTR of TNF-α among vertebrate as we observed that miR-130a-3p and -301a-3p mimics could downregulate TNF-α protein levels and reporter gene levels in both PAMs and RAW264.7 cells. [score:4]
Figure 4Omp25 upregulates miR-130a-3p, -146a, -181a, -181b, or -301a-3p in porcine alveolar macrophages (PAMs) and miR-146a, -181a, -181b, -301a-3p, or -351-5p in mouse RAW264.7 cells. [score:4]
Figure 5Upregulation of miR-130a-3p, miR-146a, miR-181a, miR-181b, miR-301a-3p, and miR-351-5p blocks LPS-stimulated TNF-α production. [score:4]
Considering that miR-130a-3p, miR-146a, miR-181a, miR-181b, miR-301a-3p, and miR-351-5p might participate in the negative regulation of TNF-α production in Omp25 -expressing cells, we measured the expression of these miRNAs in PAMs and mouse RAW264.7 cells after LV-Omp25 infection. [score:4]
We found that WT B. suis induced higher levels of miR-130a-3p, miR-146a, miR-181a, and miR-301a-3p expression than that of Δ omp25 B. suis in PAMs (Figures 8A–D). [score:3]
Given above results, we reasoned that miR-130a-3p, miR-146a, miR-181a, miR-181b, miR-301a-3p, and miR-351-5p likely play crucial roles in the Omp25 inhibition of LPS -induced TNF-α production. [score:3]
To confirm that TNF-α is regulated at posttranscriptional level by which miRNA, we constructed reporter plasmids encoding the WT 3′UTR of porcine or murine TNF-α mRNA downstream of the firefly luciferase gene (porcine or murine TNF-α WT-3′UTR), as well as parallel plasmids containing mismatches in the predicted binding sites (miR-130a-3p, miR-181a, miR-181b, miR-301a-3p, or miR-351-5p MT-3′UTR) of the 3′UTR region (Figure S5 in). [score:2]
MI0008217) and mmu-miR-130a (miRBase accession no. [score:1]
To test this, PAMs and mouse RAW264.7 cells were transfected with miRNA control, miR-130a-3p mimics, miR-146a mimics, miR-181a mimics, miR-181b mimics, miR-301a-3p mimics, or miR-351-5p mimics, and stimulated the transfected cells with LPS for 24 h. In PAMs, transfection of the mimics of miR-130a-3p, miR-146a, miR-181a, miR-181b, and miR-301a-3p decreased LPS -induced TNF-α, except miR-351-5p (Figure 5A). [score:1]
NT_039207.8) genomic DNA showed 68% identity by Clustal W method, while the 1,000 nucleotide sequences (13,37,972–13,36,973) at the upstream of ssc-miR-130a only showed 56.2% identity with the 1,000 bases region (847,40,116–847,41,115) at the upstream of mmu-miR-130a precursor. [score:1]
Moreover, we found some differences between ssc-miR-130a (miRBase accession no. [score:1]
In RAW264.7 cells, transfection of the mimics of miR-130a-3p, miR-146a, miR-181a, miR-181b, miR-301a-3p, and miR-351-5p decreased LPS -induced TNF-α (Figure 5B). [score:1]
Comparing 2,000 bases region (13,38,972–13,36,973) at the upstream of ssc-miR-130a precursor from Sscrofa 10.2 (GenBank accession no. [score:1]
NW_003609527) genomic DNA with the 2,000 bases region (847,39,116–847,41,115) at the upstream of mmu-miR-130a precursor from Mus musculus (GenBank accession no. [score:1]
showed that the levels of miR-130a-3p, miR-146a, miR-181a, miR-181b, and miR-301a-3p increased at 12–36 h in LV-Omp25-infected PAMs, whereas miR-130a-3p, miR-146a, miR-181a, miR-181b, miR-301a-3p, and miR-351-5p showed similar changes in LV-Omp25-infected RAW264.7 cells (Figures 4C–G,I–M). [score:1]
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[+] score: 189
Also, the expression of miR-130a was elevated in HDAC3-silenced or HDAC3 inhibitor -treated U251 cells, suggesting that βOHB increased the expression of miR-130a via inhibiting HDAC3 expression, at least in part. [score:11]
Unexpectedly, silencing of HDAC3 gene expression caused up-regulation of AQP4-M1 and AQP4-M23 in different degrees, suggesting that HDAC3 may regulate AQP4 gene expression by completely different mechanisms independently of miR-130a. [score:9]
To further determinate whether HDAC3 regulates miR-130a expression, siRNA duplex or specific inhibitor RGFP966 was used to interfere with endogenous HDAC3 mRNA expression in cells (Figure 9). [score:8]
In rat astrocytes primary cultures, a large proportion of AQP4-M23 protein has been reported to derive from AQP4-M1 mRNA translation, which could explain the inconsistent of alteration in AQP4-M23 mRNA and protein expression in cells treated by miR-130a mimic or miR-130a inhibitor. [score:7]
Moreover, the expression of AQP4-M1 and AQP4-M23 protein was decreased in different degrees (p < 0.05; p < 0.01), resulting in the decrease of AQP4-M1/M23 protein ratio (p < 0.01), in cells treated with miR-130a mimic, and increased in varying extent in AQP4-M1 and AQP4-M23 protein expression, leading to the increase of AQP4-M1/M23 protein ratio in cells treated with miR-130a inhibitor (p < 0.01). [score:7]
The miR-130a mimic and inhibitor were separately used to improve and inhibit miR-130a expression. [score:7]
Nevertheless, it is not clarified whether inhibiting HDAC3 regulates the expression of miR-130a and the ratio of AQP4-M1/M23 in AD. [score:6]
Silencing HDAC3 Caused the Up-regulation of miR-130a Expression and the Reduction of AQP4-M1/M23 Ratio in U251 Cells. [score:6]
HDAC3 knockdown or HDAC3 inhibition promoted the expression of miRNA-130a, and HDAC3 was recruited to the promoter region of the gene encoding miR-130a in peripheral blood mononuclear cells (Jiang and Wang, 2016). [score:6]
FIGURE 9Silencing HDAC3 caused the up-regulation of miR-130a expression and reduction of AQP4-M1/M23 ratio in U251 cells. [score:6]
After ADF intervention, a marked increase (p < 0.05) in miR-130a expression and a significant decrease (p < 0.01) in HDAC3 expression were found in APP/PS1 mice. [score:5]
FIGURE 7β-Hydroxybutyrate alleviated the decrease of miR-130a expression and the increase of HDAC3 expression in Aβ-exposed U251 cells. [score:5]
We found that the expression of AQP4-M1 mRNA was decreased in cells treated with miR-130a mimic (p < 0.05) and was increased in cells treated with miR-130a inhibitor (p < 0.01). [score:5]
βOHB Alleviated the Decrease of miR-130a Expression and the Increase of HDAC3 Expression in Aβ-Exposed U251 Cells. [score:5]
Cells exposed to Aβ had a significant decrease in miR-130a expression (Figure 7A) and a remarkable increase in HDAC3 expression (Figures 7B–D) relative to those observed in control cells (p < 0.05; p < 0.01). [score:5]
The relative expression of miR-130a (A; U6 as a reference standard), AQP4 mRNA (A; β-actin as a reference standard), and proteins (B,C) expression were, respectively, analyzed by qRT-PCR and Western blot in HDAC3-silenced cells (n = 6; mean ± SD; one-way ANOVA followed by LSD multiple comparison tests; [∗∗] p < 0.01 vs. [score:5]
Furthermore, there was a big discrepancy between the effect of mimic-miR-130a on the expression of AQP4-M1 mRNA and protein, suggesting that this mimic-miR-130a possibly influenced translation of the AQP4-M1 mRNA, rather than only transcription of the AQP4-M1 DNA coding sequence. [score:5]
FIGURE 5Alternate-day fasting alleviated the decrease of miR-130a expression and the increase of HDAC3 expression in the cerebral cortex of APP/PS1 mice. [score:5]
ADF Alleviated the Decrease of miR-130a Expression and the Increase of HDAC3 Expression in the Cerebral Cortex of APP/PS1 Mice. [score:5]
However, no difference in AQP4-M23 mRNA expression was found in cells treated with miR-130a mimic or inhibitor. [score:5]
Meanwhile, βOHB-pre -treated cells exposed to Aβ had a significant increase in miR-130a expression and an obvious decrease in HDAC3 expression relative to the levels observed in Aβ-exposed cells (p < 0.05; p < 0.01). [score:5]
The relative expression of AQP4 mRNA (A) and proteins (B,C) were analyzed by qRT-PCR (U6 as a reference standard) and Western blot, respectively, in miR-130a mimic and inhibitor -treated cells (n = 6; mean ± SD; one-way ANOVA followed by LSD multiple comparison tests; [∗] p < 0.05, [∗∗] p < 0.01 vs. [score:5]
The increase of miR-130a expression and the decrease of HDAC3 expression were observed in βOHB-pre -treated cells compared with control cells (p < 0.05). [score:4]
The results showed that the expression of miR-130a was significantly decreased (p < 0.05) and the expression of HDAC3 mRNA and protein was significantly increased (p < 0.01) in APP/PS1 mice compared with WT mice. [score:4]
Additionally, the opposite effects on the regulation of AQP4-M1/M23 ratio were obtained by using miR-130a inhibitor and miR-130a mimic. [score:4]
Further research, using miR-130a mimic, showed a decrease in the expression of AQP4-M1 instead of AQP4-M23 mRNA in vitro. [score:3]
The relative expression of miR-130a (A; U6 as a reference standard), HDAC3 mRNA (B; β-actin as a reference standard), and proteins (C,D) were analyzed by qRT-PCR and Western blot, respectively (n = 9 or 10; mean ± SD; one-way ANOVA followed by LSD multiple comparison tests; [∗] p < 0.05, [∗∗] p < 0.01 vs. [score:3]
The micrOFF [®] miRNA mimic and inhibitor for human miR-130a were designed and synthesized by Guangzhou RiboBio Co. [score:3]
In this study, the effect of miR-130a mimic on AQP4-M1 was in accordance with that of βOHB, but the opposite effects were found in the alteration of AQP4-M23 expression in cells treated with mimic and βOHB. [score:3]
The relative expression of miR-130a (A; U6 as a reference standard), HDAC3 mRNA (B; β-actin as a reference standard), and proteins (C,D) were analyzed by qRT-PCR and Western blot, respectively [n = 6; mean ± SD; one-way ANOVA followed by LSD multiple comparison tests; [∗] p < 0.05, [∗∗] p < 0.01 vs. [score:3]
As illustrated in Figure 9A, the expression of miR-130a was significantly increased in cells with HDAC3 siRNA or RGFP966 (p < 0.01). [score:3]
miR-130a mimic sequence: 5′-CAGUGCAAUGUUAAAAGGGCAU-3′, anti-sequence: 5′-GUCACGUUACAAUUUUCCCGUA-3′; and miR-130a inhibitor sequence: 5′-mAmUmGmCmCmCmUmUmUmUmAmAmCmAmUmUmGmCmAmCmUmG-3′ (mN, 2′-O-methyl ribose). [score:3]
Role of histone deacetylase 3 in ankylosing spondylitis via negative feedback loop with microRNA-130a and enhancement of tumor necrosis factor-1alpha expression in peripheral blood mononuclear cells. [score:3]
Possibly, the repression of AQP4-M1 expression by miR-130a contributed to the reduction of AQP4-M1/M23 ratio. [score:3]
To further investigate whether miR-130a alters the AQP4-M1/M23 ratio through regulating the transcriptional activity of AQP4-M1, miR-130a mimic and inhibitor were used to explore the possible mechanism in U251 cells (Figure 8). [score:2]
In addition, βOHB may partly mediate the effect of ADF on the reduction of AQP4-M1/M23 ratio in AD, in which the regulation of βOHB on miR-130a and HDAC3 may be implicated as a potential mechanism. [score:2]
The expression of AQP4 mRNA and protein, and miR-130a levels were investigated by the above methods. [score:1]
Interestingly, a study in ankylosing spondylitis found that HDAC3 formed negative feedback loop with miR-130a in peripheral blood mononuclear cells (Jiang and Wang, 2016). [score:1]
Briefly, HDAC3 may be involved in the reduction of AQP4-M1/M23 ratio induced by βOHB, and in which miR-130a may be implicated. [score:1]
Effect of miR-130a on Transcriptional Activity of AQP4 and the Ratio of AQP4-M1/M23. [score:1]
It is indicated that miR-130a partly mediated the effect of βOHB on the AQP4-M1/M23 ratio, in which other ways may be involved. [score:1]
To further investigate the possible mechanisms responsible for the role of ADF in AQP4-M1/M23 ratio, we examined the expression of miR-130a (Figure 5A) and HDAC3 (Figures 5B–D) in the cerebral cortex among groups. [score:1]
Furthermore, βOHB may at least partly mediate the effect of IF on the reduction of AQP4-M1/M23 ratio in AD, in which miR-130a and HDAC3 are possibly implicated. [score:1]
Specifically, levels of miR-130a, AQP4, and HDAC3 mRNA in cells were analyzed. [score:1]
In the current study, decreased miR-130a levels were found in the cerebral cortex of APP/PS1 mice and in Aβ-exposed U251 cells, which were alleviated by ADF and βOHB, respectively. [score:1]
After 24 h, the expression of AQP4 mRNA and protein, and miR-130a levels were investigated by the above methods. [score:1]
FIGURE 8Effect of miR-130a on transcriptional activity of AQP4 and the AQP4-M1/M23 ratio. [score:1]
miR-130a has been reported to repress transcriptional activity of AQP4-M1 but not AQP4-M23 in the study of cerebral ischemia (Sepramaniam et al., 2012). [score:1]
The transcriptional activity of AQP4-M1 was found to be repressed by microRNA-130a (miR-130a), which may result in the reduction of AQP4-M1/M23 ratio, in Astrocytoma (CRL1718) and HeLa (CCL2) cells (Sepramaniam et al., 2012). [score:1]
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[+] score: 172
Other miRNAs from this paper: mmu-mir-130b, mmu-mir-221, mmu-mir-130c
Given the importance of balanced expression and function between molecules that promote and inhibit angiogenesis in development, it is not surprising that the temporal expression of miR-221 and miR-130a is finely tuned in the developing lung. [score:8]
Given that upregulating miR-221 or downregulating miR-130a (and vice versa) in ex vivo lung cultures produce a similar branching phenotype, we wanted to elucidate whether miR-221 and miR-130a had opposing effects on the underlying vascular bed in these lungs as well. [score:7]
To begin to understand the functional roles of miR-221 and miR-130a in the developing lung, E14 ex vivo lung cultures were treated with anti-miRs to downregulate or mimics to upregulate these miRNAs. [score:7]
Both downregulation of miR-221 and upregulation of miR-130a resulted in increased vascular density, with a concomitant increase in distal airway branching (Table 2). [score:7]
Furthermore, the opposite effects were observed with miR-221 upregulation or miR-130a downregulation. [score:7]
The highly branched phenotype is similar to what was observed with miR-221 downregulation and miR-130a upregulation in the ex vivo lung cultures. [score:7]
At 24 hours of culture, lungs were randomly assigned for an additional 48 hours to the following conditions, which are summarized in Table 1: A) To inhibit specific miRNA function, antisense oligos (anti-miRs) to miR-221 or miR-130a (IDT, Coralville, IA), or anti-miR scrambled control oligo (Ambion, Grand Island, NY); B) To upregulate specific miRNA function, Pre-miR 221 (Mimic 221), Pre-miR 130a (Mimic 130a) or Pre-miR scrambled control (Ambion, Grand Island, NY) oligos. [score:6]
Upregulation of miR-221 and miR-130a was confirmed by qRT-PCR (60 to 100 fold up regulation, data not shown). [score:5]
Hoxb5 has been identified as a target of miR-221 in thyroid carcinoma, and Hoxa5 as a target of miR-130a in human umbilical vein endothelial cells (HUVEC) cells [13], [22]. [score:5]
miR-221 and miR-130a Target Expression of Hox Proteins. [score:5]
Importantly, the opposing effects on angiogenesis of miR-221 and miR-130a and their respective targets Hoxb5 and Hoxa5, and the functions of Hoxb5 and Hoxa5 on airway morphogenesis suggests that these miRNAs and Hox proteins control both lung blood vessel and airway development. [score:4]
Upregulation of miR-221 (blue bar) and miR-130a (red bar) was confirmed by qRT-PCR. [score:4]
Downregulation of miR-221 (blue bar) and miR-130a (red bar) was confirmed by qRT-PCR. [score:4]
We were unable to identify direct targets for either miR-221 or miR-130a in the lung endothelial cells. [score:4]
These ex vivo and in vitro studies show that miR-221 and miR-130a mediate their effects on lung development partly through targeting the developing vasculature. [score:4]
A dose response was done in MFLM-91U cells to confirm that 1 nM of Mimic upregulated miR-221 levels by 100 fold and miR-130a levels by 20 fold. [score:4]
miR-221 and miR-130a Target Angiogenesis in vitro. [score:3]
These results suggest that miR-221 and miR-130a target the developing lung vasculature and are consistent with reports that miR-221 is anti-angiogenic and mir-130a is pro-angiogenic. [score:3]
Exogenous miR-130a has been shown to reduce Hoxa5 protein expression in HUVEC cells [13]. [score:3]
Several groups have shown that miR-221 and miR-130a regulate endothelial cell function, suggesting that regulation of these miRNAs in the embryonic lung vasculature may also affect airway branching morphogenesis [10]. [score:3]
In this study we show for the first time that miR-221 and miR-130a regulate both airway branching and lung microvascular development. [score:3]
Mir-221 and miR-130a are reported to target two Hox genes known to have important functions in embryonic lung branching morphogenesis and epithelial cell fate [14]– [21]. [score:3]
To address whether miR-221 and miR-130a altered neovascularization by directly targeting fetal lung endothelial cells, we utilized an in vitro angiogenesis assay. [score:3]
Total miR-130a expression levels decreased at E16 and E17 before increasing at E18 to levels seen at E15 (Figure 2A). [score:3]
Reported targets of miR-221 and miR-130a in other cell types mostly include downstream signaling molecules and transcription factors which were not present in this array [39], [40]. [score:3]
miR-221 and miR-130a alter localization of Hox protein expression. [score:3]
Several studies describe promotion or suppression of angiogenesis by specific microRNAs, including miR-221 and miR-130a. [score:3]
This concept is further supported by our previously published work on the expression and function of these Hox proteins in the developing lung and the phenotype observed when miR-221 and miR-130a are manipulated [16], [34]. [score:3]
In contrast, miR-130 is pro-angiogenic, promoting endothelial cell proliferation and migration by inhibiting anti-angiogenic homeobox proteins [13]. [score:3]
MiR-221 inhibited endothelial cell tube formation and migration, whereas miR-130a enhanced tube and vascular plexus formation and cell migration. [score:3]
Taken together, analysis of miR-221 and miR-130a distribution in the developing lung suggests functional roles in the progression of lung development. [score:2]
miR-221 and miR-130a Regulate Branching Morphogenesis. [score:2]
Several studies have highlighted the role of miR-221 and miR-130a in regulating endothelial cell biology for angiogenesis, showing that miR-221 has angiostatic and miR-130a has pro-angiogenic properties [10]. [score:2]
miR-221 and miR-130a are Temporally and Spatially Regulated Across Gestation. [score:2]
Different from miR-221, miR-130a expression was more intense in the epithelium (arrowhead) compared to the mesenchyme at E16 (arrows). [score:2]
Some of the opposing airway branching phenotypes created by perturbations of miR-221 and miR-130a could be due to regulation of an epithelial mechanism controlling the progression of branching morphogenesis. [score:2]
MiR-221 and miR-130a are present in multiple cellular compartments during lung development, as shown by the in situ hybridization results. [score:2]
These studies show that miR-221 and miR-130a can alter vascularization by directly affecting endothelial cell behavior resulting in changes in tube formation and cell migration. [score:2]
Our present study used ex vivo and in vitro mo dels to explore how miR-221 and miR-130a regulate airway and vascular branching in the lung. [score:2]
In summary, we have shown that miR-221 and miR-130a coordinately regulate airway and vascular branching. [score:2]
These results suggest a regulatory role for miR-221 and miR-130a on Hoxb5 and Hoxa5, respectively, in developing lung. [score:2]
miR-221 and miR-130a Regulate Neovascularization During Lung Branching Morphogenesis. [score:2]
We propose that miR-221 and miR-130a actively participate in regulation of embryonic lung vascular and airway branching. [score:2]
These studies suggest that miR-130a may be involved in expanding proximal progenitors in the developing lung. [score:1]
Effect of miR-130a and miR-221 on Epithelial Cell Fate And Morphology. [score:1]
To investigate the temporal and spatial expression of miR-221 and miR-130a in the developing lung, qRT-PCR and in situ hybridzation were done on mouse fetal lungs. [score:1]
Changes in total miR-221 and miR-130a were verified by qRT-PCR to ensure transfection efficiency (Figure 3A, 3D). [score:1]
The opposite phenotypes were observed when lungs were transfected with mimics to miR-221 and miR-130a. [score:1]
0055911.g002 Figure 2(A) Quantification of total miR-130a levels in gestational days E15– E18 mouse fetal lungs was done by qRT-PCR. [score:1]
Summary of phenotypes observed when ex vivo lung cultures were treated with anti-miRs or mimics to miR-221 and miR-130a. [score:1]
miR-130a temporal, spatial and cellular localization changes with advancing gestation. [score:1]
We found that increased miR-221 or decreased miR-130a levels in lung cultures produced a disorganized vascular network that was associated with reduced airway branching. [score:1]
Summary and explanation of all miR-221 and miR-130a manipulations used in experiments. [score:1]
By E18, miR-130a was restricted to the terminal bronchioles (arrowhead) and mesenchymal cell clusters around developing saccules (arrow). [score:1]
We used ex vivo and in vitro culture mo dels to identify the phenotypic function of miR-221 and miR-130a in branching morphogenesis and neovascularization of the developing lung. [score:1]
These observations provide insight into the mechanisms underlying similarities and differences in airway branching observed with miR-221 and miR-130a manipulation. [score:1]
Our findings with regards to the angiostatic properties of miR-221 and pro-angiogenic properties of miR-130a are consistent with studies of these miRNAs in human venous or lymphatic endothelial cells [11]– [13], [35]. [score:1]
These results are consistent with the current knowledge that miR-221 is anti-angiogenic and miR-130a is pro-angiogenic. [score:1]
Manipulation of miR-221 and miR-130a levels caused spatial and cellular changes in Hoxb5 and Hoxa5 localization, respectively. [score:1]
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[+] score: 136
For example, TNF-α can activate NF-κB activity to upregulate miR-130a, which in turn targets and inhibits TNF-α expression as a negative feedback loop. [score:10]
However, none of the predicted target genes of miR-130a were found to be potential indirect regulators of Nkd2 (data not shown), and 5′-UTR of Nkd2 was also not found to be targeted by miR-130a using TargetscanHuman 7.1 [2]. [score:9]
Subsequently, we found that miR-130a could repress the expression level of Nkd2, which could be up-regulated by curcumin. [score:6]
Here our results proposed that Wnt pathway might be a potential target for miR-130a in colon cancer, but its direct target still needs to be identified in further work. [score:6]
This process was regulated by repressing the expression of microRNA (miR)-130a, and overexpressing miR-130a could completely abolish the curcumin -induced anti-tumor activity in colon cancer. [score:6]
Therefore, we overexpressed miR-130a in SW480 cells and treated the cells with curcumin, followed by determining cell proliferation and β-catenin expression level. [score:5]
However, none of the predicted target genes of miR-130a were found to be potential indirect regulators of Nkd2, therefore the exact mechanism under this inhibition still elusive, and further investigations are warranted. [score:5]
Taken together our earlier clinical study where high miR-130a expression level was significantly associated with poor clinical outcome (Kara et al., 2015), results in our current study suggests that when agent like curcumin is used to treat colon cancer, therapies inhibiting miR-130a may be combined for better clinical efficacy. [score:5]
Curcumin suppresses colon cancer by inhibiting Wnt/β-catenin pathway via miR-130a. [score:5]
Upregulated miR-130a increases drug resistance by regulating RUNX3 and Wnt signaling in cisplatin -treated HCC cell. [score:5]
Among these miRNAs, miR-130a may be important for cancer formation because overexpressing miR-130a could restore the proliferation of curcumin -suppressed cancer cells back to normal. [score:5]
These results indicated that curcumin inhibited the Wnt signaling by repressing the expression level of the miR-130a. [score:5]
These results indicated that curcumin suppressed the Wnt/β-catenin pathway via inhibiting miR-130a. [score:5]
These results suggested that miR-130a may regulate the Wnt pathway by inhibiting Nkd2. [score:4]
q-PCR showed that with curcumin treatment, miR-21 and miR-130a were down-regulated (Figure 4). [score:4]
It has been reported that miR-130a expression is disregulated in several types of cancer (Zhang et al., 2017), including colon cancer (Kara et al., 2015). [score:4]
We also predicted the targets of miR-130a through online tool [1], among which LPR6 was identified to be related to the Wnt pathway. [score:3]
We overexpressed miR-130a in SW480 cells and treated them with curcumin. [score:3]
Increasing targets of miR-130a have been identified. [score:3]
Our study supports miR-130a as a novel target in the treatment of colon cancer. [score:3]
NF-kappaB-modulated miR-130a targets TNF-alpha in cervical cancer cells. [score:3]
Therefore, we tested the level of LPR6 after miR-130a overexpression in the absence or presence of curcumin treatment. [score:3]
FIGURE 5Curcumin inhibited Wnt pathway via miR-130a. [score:3]
However, little is known about the targets of miR-130a in colon cancer. [score:3]
Curcumin Suppressed the Wnt/β-Catenin Pathway via miR-130a. [score:3]
Our results showed that miR-130a could repress the expression of Nkd2 in both mRNA and protein levels (Figures 6A,C). [score:3]
MiR-130a may serve as a new target for CRC treatment. [score:2]
This negative feedback regulation of NF-κB/miR-130a/TNF-α/NF-κB may provide insight into the carcinogenesis of cervical cancer (Zhang et al., 2014). [score:2]
We therefore examined the miRNAs reported to be involved in colon cancer, and found that only miR-21 and miR-130a were affected by curcumin. [score:1]
Furthermore, we tested the serum level of miR-130a in the experimental mice. [score:1]
We found that the short-lived mice had higher level of miR-130a in their serum than the long-lived mice. [score:1]
Since miR-130a was a novel miRNA that had few reported functions in colon cancer, we focused on the role of miR-130a in curcumin action in colon cancer. [score:1]
These data suggested that miR-130 might act to antagonize curcumin’s anti-tumor effect. [score:1]
The serum level of miR-130a was significantly higher in the short-lived group than that of the long-lived group of mice (Figure 7), which confirmed that miR-130a functioned to antagonize curcumin’s anti-tumor effect. [score:1]
This suggested that miR-130a might contribute to the resistance of colon cancer cells to chemotherapy. [score:1]
In the presence of miR-130a, cell proliferation was restored to similar level as the control cells. [score:1]
The role of miR-130a in cancer. [score:1]
Interestingly, in the presence of miR-130a, cell proliferation was restored to similar level as the control group (Figure 5A), and β-catenin level was also returned to normal level (Figure 5B). [score:1]
We therefore examined the serum level of miR-130a in mice treated with curcumin. [score:1]
MiR-130a also increases drug resistance by regulating RUNX3 and Wnt signaling in cisplatin -treated hepatocellular carcinoma cells (Xu et al., 2012). [score:1]
MiR-21 has been reported to be involved in colon cancer, whereas the function of miR-130a is not clear. [score:1]
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8
[+] score: 45
In order to demonstrate the potential linkage of YAP/miR-130a/KLF4 with apicidin -induced cardiac commitment, the expression level of YAP, KLF4, or GATA4 was assessed in MSC after apicidin treatment, YAP knockdown, or miR-130a inhibition. [score:6]
KLF4 is one of the targets of miR-130a [28], and we previously reported that angiogenic activity was declined in KLF4 upregulated MSC [29]. [score:6]
Furthermore, miR-130a was identified as one of the downstream effectors of YAP, which resulted in retarded angiogenesis and GATA4 upregulation (Figure 7). [score:4]
Besides, miR-130a-reduced MSC showed the upregulations of both KLF4 and GATA4 (Figure 7E). [score:4]
To test whether miR-130a was involved in apicidin -induced cardiac commitment of MSC, the expression level of miR-130a was assessed in AC/MSC and YAP knockdown MSC. [score:4]
Tube formation was also decreased in miR-130a reduced MSC (Figure 7C), and this result suggested that apicidin -induced YAP suppression might result in miR-130a reduction. [score:3]
To examine whether miR-130a was related with cardiac marker induction in MSC, mRNA levels of cardiac-specific markers was assessed in miR-130a inhibitor -transfected MSC. [score:3]
To understand the mechanism of YAP suppression -induced cardiac marker inductions in AC/MSC, we came across miR-130a, which was recently reported to be induced by YAP, and also identified as a driver of endothelial differentiation [26, 27]. [score:3]
The levels of mRNA of GATA4, Nkx2.5, and cTnI were markedly increased in miR-130a inhibited MSC (Figure 7B). [score:3]
We observed the significant reduction of miR-130a by both apicidin treatment and YAP knockdown in MSC (Figure 7A). [score:2]
Figure 7 (A) miR-130a was reduced by both apicidin treatment and YAP knockdown in MSC (n=4). [score:2]
miR-130a and KLF4 are involved in apicidin -induced cardiac commitment of MSC. [score:1]
Apicidin -induced cardiac commitment of MSC involves miR-130a and KLF4. [score:1]
These results signified that apicidin may determine the cell fate toward cardiac lineage through YAP/miR-130a/KLF4 in MSC (Figure 7F). [score:1]
MiRNA-control (miR-con) and miRNA-130a were purchased from Dharmacon (GE HearthCare Life Science, USA). [score:1]
Our results demonstrated that apicidin treatment is clearly involved in cardiogenic gene transcription program and associated with cardiac commitment of MSC, and allow better understanding of the mechanism of cardiac commitment of MSC, although the YAP/miR-130a-related signaling networks remain to be addressed (Figure 8). [score:1]
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9
[+] score: 24
Analysis of global profiles of miRNA expression in skeletal muscle with microarray shows that expression of 4 miRNAs (miR-29a, miR-29b, miR-29c and miR-150) are up-regulated [23], whereas expression of 11 miRNAs (miR-379, miR-127, miR299-5p, miR-434-3p, miR-335, miR130a, miR-19b, miR-451, miR-148a, miR-199a and miR-152) are down-regulated in skeletal muscle of type 2 diabetic rats [23]. [score:13]
For example, it has been shown that expression of 4 miRNAs (miR-29a, miR-29b, miR-29c and miR-150) is up-regulated [23], whereas expression of 11 miRNAs (miR-379, miR-127, miR299-5p, miR-434-3p, miR-335, miR130a, miR-19b, miR-451, miR-148a, miR-199a and miR-152) is down-regulated in skeletal muscle of type 2 diabetic rats [23]. [score:11]
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[+] score: 24
Our data indicated that miR-130a levels were upregulated by flutamide on GD 18.0. [score:4]
In contrast, downregulation of miR-130a with an anti-miR led to reduced airway branching in the lung explant [36]. [score:4]
Upregulation of miR-130a was shown to increase vascular density and distal airway branching [36]. [score:4]
miR-130a was shown to be expressed in murine fetal lung, where a decrease in miR-130a levels was observed from GD 15.0 to GD 17.0, followed by an increase up to GD 18.0 [36]. [score:3]
One putative miR-130a target is cAMP response element binding protein 1 (Creb1) mRNA. [score:3]
Another putative target of miR-130a is Zeb2 mRNA. [score:3]
Our data suggest that androgens exert both a positive pressure on the expression of Creb1 and a negative pressure on vascularization and distal airway branching on GD 18.0 through miR-130a. [score:3]
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[+] score: 22
Lee E. K. Lee M. J. Ab delmohsen K. Kim W. Kim M. M. Srikantan S. Martindale J. L. Hutchison E. R. Kim H. H. Marasa B. S. miR-130 Suppresses Adipogenesis by Inhibiting Peroxisome Proliferator-Activated Receptor γ Expression Mol. [score:7]
These include the miR-130 family members that repress brown and white adipogenesis via direct inhibition of Pparg [30] and miR-378 that activates Cebpa and Cebpb expression during adipogenesis and enhances brown fat expansion [31, 32]. [score:6]
Expression of miR-130 is increased in adipocyte hypertrophy and fat inflammation [41] and interestingly, miR-130 of the current Fto- KO BAT was significantly decreased in comparison with WT, indicating a role for FTO in the regulation of miR-130 and the pathophysiology of obesity. [score:4]
PPARγ and C/EBPβ are important transcription factors in both brown and white adipogenesis and are inhibited by miR-130 and miR-155, respectively [30, 33]. [score:3]
Kim C. Lee H. Cho Y. M. Kwon O. J. Kim W. Lee E. K. TNFα-Induced miR-130 Resulted in Adipocyte Dysfunction during Obesity-Related Inflammation FEBS Lett. [score:1]
In addition, miR-130 was reported to be increased in WAT of mice due to HFD [41], which was also observed in our WT mice but not in the Fto- KO mice. [score:1]
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[+] score: 20
On the basis that YAP can directly promote miRNA-130a transcription and inhibit VGLL4 expression [32], we hypothesized that YAP inhibited 14-3-3ζ gene translation by first expressing some miRNAs. [score:12]
Shen et al. reported that YAP directly induced miRNA-130a expression to inhibit VGLL4 expression [32]. [score:8]
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13
[+] score: 17
It is important to note that only 9 miRNAs (miR-100-5p, miR-130a-5p, miR-146b-3p, miR-147-3p, miR-151-5p, miR-155-3p, miR-223-3p, miR-301a-3p, and miR-495-3p) were significantly upregulated or downregulated in both lungs infected with either wild type w81 or the mouse-adapted ma81 strain at all time points (Tables  1 and 2). [score:7]
Twenty-seven and 20 differentially expressed miRNAs identified to be commonly presented at 1 and 3 dpi were presented in Tables  3 and 4. Of these, only miR-100-5p, miR-130a-5p, miR-146b-3p, miR-147-3p, miR-151-5p, miR-155-3p, miR-223-3p, miR-301a-3p, and miR-495-3p were commonly upregulated at both 1 and 3 dpi. [score:6]
It is noteworthy that only 9 miRNAs (miR-100-5p, miR-130a-5p, miR-146b-3p, miR-147-3p, miR-151-5p, miR-155-3p, miR-223-3p, miR-301a-3p, and miR-495-3p) were significantly upregulated in both lungs infected with either wild type w81 or the mouse-adapted ma81 strain at both time points. [score:4]
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14
[+] score: 16
Furthermore, qPCR was performed again to validate the downregulated and upregulated expression of selected miRNAs that may be relevant to development and confirmed that miR-135, miR-302, miR-449a, miR-200b, miR-200c, miR-193b, miR-130, and miR-141 were downregulated, whereas miR-10a, miR-181, and miR-470 were upregulated by RA treatment (Fig 4C and 4D). [score:16]
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[+] score: 16
Similar to our observation of MS-exposure-related suppression in A/J lung tumors, miR-130a expression was also found to be down-regulated in airway epithelial cells of healthy smokers compared to levels observed in non-smokers (Schembri et al., 2009) and in lung organotypical cultures exposed to MS (Mathis et al., 2013). [score:7]
These findings suggest that miR-130a transcription in the lung is modulated by cigarette smoke exposure and that deregulation of its activity may contribute to smoking -induced lung disease. [score:4]
Further, reduced miR-130a expression has been observed in non-small cell lung carcinoma (NSCLC) cell lines (Acunzo et al., 2012) and squamous cell carcinomas of the lung (Gao et al., 2011). [score:3]
Interestingly, of the 3 miRNA that were affected by cigarette smoke exposure in tumors only, mmu-miR-151-3p, mmu-miR-130a-3p and mmu-miR-184-3p have previously been implicated in carcinogenesis. [score:1]
Surprisingly, the effects of cigarette smoke on miRNA levels were greater in parenchymal tissues than in tumors (Figure 5 and 7), and miRNA were distributed across three major categories of unequal sizes: 62 mRNA were altered (raw p-values were smaller than 0.05 for the corresponding pairwise comparisons) in parenchyma only, 3 miRNA (mmu-miR-130a-3p, mmu-miR-151-3p, mmu-miR-184-3p) were altered in tumors only and 5 in both tumor and parenchyma. [score:1]
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16
[+] score: 15
Other miRNAs from this paper: mmu-mir-196a-1, mmu-mir-196a-2, mmu-mir-1271
HOXA5 downregulation in endothelial cells is mediated by the microRNA-130a that specifically targets a consensus sequence in the 3′-UTR of the HOXA5 transcript [94]. [score:6]
Yang F. Miao L. Mei Y. Wu M. Retinoic acid -induced HOXA5 expression is co-regulated by HuR and miR-130a Cell. [score:4]
For example, RA treatment decreases miR-130a levels, which derepress HOXA5 translation. [score:3]
miR-130a is frequently cited to contribute to Hoxa5 post-transcriptional regulation. [score:2]
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[+] score: 14
miR-130a was largely responsible for the down-regulation of GAX expression in response to mitogens and pro-angiogenic factors and antagonised the antiangiogenic activity of GAX [26]. [score:6]
Regulation of angiogenesis through a microRNA (miR-130a) that down-regulates antiangiogenic homeobox genes GAX and HOXA5. [score:5]
Chen and Gorski did an in silico search for micro -RNA binding sites in the GAX 5’UTR and identified consensus sites for multiple candidate micro -RNAs, of which only miR-130a was expressed in proliferating endothelial cells [26]. [score:3]
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[+] score: 13
The predicted sites for miR-130 and miR-17/20 within the Cd69 3' UTR also affected eGFP reporter gene expression in DP thymocytes. [score:3]
However, deletion of the miR-130 and particularly the miR-17/20 site resulted in increased eGFP expression in wild type CD4+ T cells (Fig. 3C). [score:3]
A dual fluorescence reporter system identifies endogenous microRNAs that target the Cd69 3'UTR in DP thymocytesThe Cd69 3'UTR contains predicted sites for miR-181, miR-130 and miR-17/20 (http://www. [score:3]
org) and there is firm experimental evidence for Cd69 regulation by miR-181a, miR-130 and the miR-17-92 cluster (which encodes the microRNAs miR-17, -18, -19a, -19b, -20a, and -92 [34] in T lymphocytes [31– 33]. [score:2]
The Cd69 3'UTR contains predicted sites for miR-181, miR-130 and miR-17/20 (http://www. [score:1]
The 842 nt 3’ UTR of Cd69 contains predicted binding sites for miR-181, miR-130 and miR-17-20 starting at positions 255, 354 and 391, respectively, which were mutated alone and in combination. [score:1]
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[+] score: 13
Among the list, members of the miR-29 family, miR-203, miR-762, and miR-1224, showed upregulation, whereas members of the miR-107 family, miR-127 and miR-130a/b, miR-342-3p, miR-351, miR-379, miR-455, and miR-467a, were downregulated in both strains. [score:7]
miRNAs that were differentially expressed only in the LW during aging include miR-29c, miR-705, miR-99a, miR-127, miR-130a, miR-145, miR-151-5p, miR-379, miR-467a, and miR-574-3p. [score:3]
miRNA-130a is oncogenic, contributing to colon tumorigenesis by regulating TGF-β/Smad signaling [47]. [score:2]
These miRNAs include miR-107, miR-127, miR-130a/b, miR-145, miR-342, miR-351, miR-379, miR-455, and miR-467. [score:1]
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[+] score: 13
For example, miR-22, miR-142-3p and miR-142-5p were upregulated in CD11c [+] CD11b [+] B220 [−] cDCs and downregulated in pDCs relative to progenitor expression levels, while miR-20a, miR-17-5p and miR-130a showed the reverse pattern. [score:9]
However, inspection of the human IRF8 3′UTR revealed potential target sites for multiple miRNAs, including miR-130a, miR-19a and miR-19b, which are differentially regulated in mouse pDCs and cDCs (results herein). [score:4]
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[+] score: 12
Interestingly, some of the lens-enriched miRNAs are expressed at significant levels in the cornea (Figure 1D) and by ISH we frequently observe concurrent lens and cornea miRNA expression (e. g. miR-130a, miR-149, miR-883b-5p; red arrowheads in Figure 6), probably reflecting the common origin of these epithelial tissues. [score:5]
Collectively, our results confirm the cornea expression of miRNAs already reported in literature [27, 31, 32] and reveal the corneal-enrichment of others that had not been previously described to be expressed in the eye (e. g. miR-130a, miR-130b, miR-132, miR-129-3p, the miR-200 family, miR-468, miR-874). [score:5]
For miR-130a, miR-149 and miR-883b-5p concomitant staining of the corneal epithelium can be seen (red arrowheads). [score:1]
From the latter group, 11 stained clearly both the corneal epithelium (red arrowheads) and endothelium (blue arrowheads, right column in Figure 5B; Database) while the remaining ones (e. g. miR-106a, miR-130a, miR-132, miR-494, miR-31) were detected only in the epithelium (left column in Figure 5B; Database). [score:1]
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[+] score: 12
On the other hand, the down-regulation of mmu-miR-122 and mmu-miR-130a during HFD -induced obesity that we report has not been described before. [score:4]
On the contrary, the following miRNAs were down-regulated in WAT after HFD feeding: mmu-miR-141, mmu-miR-200a, mmu-miR-200b, mmu-miR-200c, mmu-miR-122, mmu-miR-204, mmu-miR-133b, mmu-miR-1, mmu-miR-30a*, mmu-miR-130a, mmu-miR-192, mmu-miR-193a-3p, mmu-miR-203, mmu-miR-378 and mmu-miR-30e*. [score:4]
The following 22 murine microRNAs were selected for qPCR validation of their expression: mmu-miR-1, mmu-miR-21, mmu-miR-30a*, mmu-miR-30e*, mmu-miR-122, mmu-miR-130a, mmu-miR-133b, mmu-miR-141, mmu-miR-142-3p, mmu-miR-142-5p, mmu-miR-146a, mmu-miR-146b, mmu-miR-192, mmu-miR-193a-3p, mmu-miR-200b, mmu-miR-200c, mmu-miR-203, mmu-miR-204, mmu-miR-222, mmu-miR-342-3p, mmu-miR-378 and mmu-miR-379. [score:3]
Similarly, mmu-miR-130a is known to be a pro-angiogenic miRNA and its role in adipose tissue has not been described before [54]. [score:1]
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23
[+] score: 12
There are also a number of miRNAs such as miR-132, miR-212, miR-130a and miR-152 shown to be upregulated in the pancreatic islets of the wi dely-studied T2D mo del Goto-Kakizaki rats (Esguerra et al., 2011) with active roles in beta cell stimulus-secretion coupling (Malm et al., 2016; Ofori et al., 2017). [score:4]
Expression of miR-200a, miR-130a and miR-152 in INS-1 832/13 cells (A–C) or in EndoC-βH1 cells (D–F) at different confluences. [score:3]
For miR-200a, miR-130a and miR-152, the expression levels were found not to be influenced by cellular confluence (Fig. S2). [score:3]
We also investigated the influence of confluence on the expression levels of miR-200a, miR-130a, miR-152, miR-132 and miR-212. [score:1]
The following primers from TaqMan [®] Gene Expression and TaqMan [®] miRNA Assays were used for qPCR: Cav1/CAV1 (Rn00755834_m1/Hs00971716_m1), Aifm1/AIFM1 (Rn00442540_m1/ Hs00377585_m1), miR-375 (TM_ 000564), miR-200a (TM_000502), miR-130a (TM_00454), miR-152 (TM_000475), miR-132 (TM_000457) and miR-212 (TM_002551) were used for qPCR. [score:1]
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[+] score: 11
miR-27a and miR-130 suppress adipogenesis by inhibiting PPARγ (Kajimoto et al, 2006), whereas miR-143 induces adipogenesis by downregulating ERK5 (Esau et al, 2004). [score:8]
Several miRNAs, including miR-27a, miR-130 and miR-143, were previously shown to regulate adipogenesis. [score:2]
Recently, miRNAs in adipocytes have been shown to alter cell proliferation (the miR-24-1, miR-31 and miR-17-92 cluster) (Sun et al, 2009; Wang et al, 2008), repress Wnt signalling (miR-8) (Kennell et al, 2008), or repress peroxisome proliferator-activated receptor γ (PPARγ; miR-27a, miR-27b and miR-130) (Karbiener et al, 2009; Kim et al, 2010; Lin et al, 2009). [score:1]
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25
[+] score: 10
For instance, the transcriptional factor MAFB (V-maf musculoaponeurotic fibrosarcoma oncogene homolog B) is up-regulated during megakaryocyte differentiation upon a significant reduction of miR-130a [15]; miR-155 is also down-regulated which is accompanied by an increase in the expression of Ets-1 and Meis1 (Meis homeobox 1), two transcriptional factors that are important for megakaryocyte development [18]. [score:10]
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[+] score: 10
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-20a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-27a, hsa-mir-92a-1, hsa-mir-92a-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-15b, mmu-mir-23b, mmu-mir-27b, mmu-mir-133a-1, mmu-mir-140, mmu-mir-24-1, hsa-mir-196a-1, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, mmu-mir-206, hsa-mir-30c-2, hsa-mir-196a-2, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-200b, mmu-mir-301a, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-15b, hsa-mir-23b, hsa-mir-27b, hsa-mir-130a, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-140, hsa-mir-206, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-196a-1, mmu-mir-196a-2, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-18a, mmu-mir-20a, mmu-mir-24-2, mmu-mir-27a, mmu-mir-92a-2, hsa-mir-200c, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-17, mmu-mir-19a, mmu-mir-200c, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-19b-1, mmu-mir-92a-1, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-301a, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, hsa-mir-196b, mmu-mir-196b, dre-mir-196a-1, dre-mir-199-1, dre-mir-199-2, dre-mir-199-3, hsa-mir-18b, dre-let-7a-1, dre-let-7a-2, dre-let-7a-3, dre-let-7a-4, dre-let-7a-5, dre-let-7a-6, dre-let-7b, dre-let-7c-1, dre-let-7c-2, dre-let-7d-1, dre-let-7d-2, dre-let-7e, dre-let-7f, dre-let-7g-1, dre-let-7g-2, dre-let-7h, dre-let-7i, dre-mir-1-2, dre-mir-1-1, dre-mir-15a-1, dre-mir-15a-2, dre-mir-15b, dre-mir-17a-1, dre-mir-17a-2, dre-mir-18a, dre-mir-18b, dre-mir-18c, dre-mir-19a, dre-mir-20a, dre-mir-23b, dre-mir-24-4, dre-mir-24-2, dre-mir-24-3, dre-mir-24-1, dre-mir-27a, dre-mir-27b, dre-mir-27c, dre-mir-27d, dre-mir-27e, dre-mir-30c, dre-mir-92a-1, dre-mir-92a-2, dre-mir-92b, dre-mir-130a, dre-mir-133a-2, dre-mir-133a-1, dre-mir-133b, dre-mir-133c, dre-mir-140, dre-mir-196a-2, dre-mir-196b, dre-mir-200a, dre-mir-200b, dre-mir-200c, dre-mir-206-1, dre-mir-206-2, dre-mir-301a, dre-let-7j, hsa-mir-92b, mmu-mir-666, mmu-mir-18b, mmu-mir-92b, mmu-mir-1b, dre-mir-196c, dre-mir-196d, mmu-mir-3074-1, mmu-mir-3074-2, hsa-mir-3074, mmu-mir-133c, mmu-let-7j, mmu-let-7k, dre-mir-24b
miRNA Embryonic age Expression profile mir15a 48 and 72 hpf Midbrain, MHB, notochord mir15b 48 and 72 hpf Midbrain, neurocranium, notochord mir23b 30, 48, and 72 hpf Somites, lens, pharyngeal arches, notochord mir27b 48 and 72 hpf mir30c 48 and 72 hpf Brain, neurocranium, eye, heart mir130a 48 and 72 hpf Brain, gut tube, heart, eye mir133b 30, 48, and 72 hpf Notochord mir301a 48 and 72 hpf Forming cartilage Midbrain, neurocranium, eye, trigeminal ganglia Figure 5 Expression of mir23b in zebrafish embryos. [score:5]
miRNA Embryonic age Expression profile mir15a 48 and 72 hpf Midbrain, MHB, notochord mir15b 48 and 72 hpf Midbrain, neurocranium, notochord mir23b 30, 48, and 72 hpf Somites, lens, pharyngeal arches, notochord mir27b 48 and 72 hpf mir30c 48 and 72 hpf Brain, neurocranium, eye, heart mir130a 48 and 72 hpf Brain, gut tube, heart, eye mir133b 30, 48, and 72 hpf Notochord mir301a 48 and 72 hpf Forming cartilage Midbrain, neurocranium, eye, trigeminal ganglia Figure 5 Expression of mir23b in zebrafish embryos. [score:5]
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27
[+] score: 9
S60289 24790458 8. Zhang X. Huang L. Zhao Y. Tan W. Downregulation of miR-130a contributes to cisplatin resistance in ovarian cancer cells by targeting X-linked inhibitor of apoptosis (XIAP) directly Acta Biochim. [score:9]
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Regulation of angiogenesis through a microRNA (miR-130a) that down-regulates antiangiogenic homeobox genes GAX and HOXA5. [score:5]
HoxA5 expression can be attenuated by mir130a, which is induced by VEGF, as well as inflammatory factors [40] which likely contribute to loss of endogenous HoxA5 in tumor -associated vasculature. [score:3]
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Mature ID Fold Regulation miR-135b −2.6965 miR-363 −2.5995 miR-98 −2.543 miR-132 −2.355 miR-103 −2.1776 miR-99b −2.044 miR-135a −1.8734 let-7d −1.7861 miR-130a −1.6538 miR-152 −1.6246 miR-129-5p −1.6232 miR-298 −1.6169 miR-185 −1.6035 miR-214 −1.5746 miR-140 −1.5688 miR-134 −1.5667 miR-18b −1.5607 miR-194 −1.5509 let-7f −1.5107 miR-149 −1.51 Because miRNAs typically regulate translation in animal cells, we compared CXCL10 and STAT1 protein levels in both control and Dicer [d/d] animals and cells. [score:4]
Mature ID Fold Regulation miR-135b −2.6965 miR-363 −2.5995 miR-98 −2.543 miR-132 −2.355 miR-103 −2.1776 miR-99b −2.044 miR-135a −1.8734 let-7d −1.7861 miR-130a −1.6538 miR-152 −1.6246 miR-129-5p −1.6232 miR-298 −1.6169 miR-185 −1.6035 miR-214 −1.5746 miR-140 −1.5688 miR-134 −1.5667 miR-18b −1.5607 miR-194 −1.5509 let-7f −1.5107 miR-149 −1.51 A. Scatterplot showing relative expression of miRNAs by macroarray. [score:4]
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Our miRNA expression microarray and validation experiments, conducted on serum exosome samples, identified four miRNA seed sequences that corresponded significantly to RI mice (miR-34b-3p, miR-3082-5p, miR-130a and miR-1912), and two miRNA seed sequences that corresponded significantly to CI mice (miR-690 and miR-223). [score:3]
In contrast, only four miRNA seed sequences specific to RI mice were successfully validated for differential expression using quantitative RT-PCR as shown in Fig 6 (miR-34b-3p, miR-3082-5p, miR-130a and miR-1912). [score:3]
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Interestingly, in our studies IBD -associated microRNA-130, -195, -196, -223, -375 were down-regulated in Tregs or naive T-cells after isotretinoin treatment, indicating that isotretinoin does not induce a microRNA expression pattern similar to the one observed in IBD patients. [score:6]
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Microarray analysis showed altered expression of some miRNAs in hepatomas such as let-7a, miR-21, miR-23, miR-130, whereas the hepato-specific miR-122a and others were found downregulated in 70% of HCCs and in HCC-derived cell lines [20], [46], [47], as reported in our data (Table 1). [score:6]
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O [3] revealed upregulation of both miR-9-5p and miR-130a-3p, which are known for targeting SOCS5 and altering macrophage polarization, respectively [63, 64]. [score:6]
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Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-20a, hsa-mir-22, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-98, hsa-mir-101-1, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-15b, mmu-mir-101a, mmu-mir-126a, mmu-mir-133a-1, mmu-mir-142a, mmu-mir-181a-2, mmu-mir-194-1, hsa-mir-208a, hsa-mir-30c-2, mmu-mir-122, mmu-mir-143, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-181a-1, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-15b, hsa-mir-122, hsa-mir-130a, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-142, hsa-mir-143, hsa-mir-126, hsa-mir-194-1, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-208a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-18a, mmu-mir-20a, mmu-mir-22, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-29c, mmu-mir-98, mmu-mir-326, rno-mir-326, rno-let-7d, rno-mir-20a, rno-mir-101b, mmu-mir-101b, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-181b-2, mmu-mir-17, mmu-mir-19a, mmu-mir-181a-1, mmu-mir-26a-2, mmu-mir-19b-1, mmu-mir-181b-1, mmu-mir-181c, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-101-2, hsa-mir-26a-2, hsa-mir-378a, mmu-mir-378a, hsa-mir-326, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-181b-2, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-15b, rno-mir-16, rno-mir-17-1, rno-mir-18a, rno-mir-19b-1, rno-mir-19a, rno-mir-22, rno-mir-26a, rno-mir-26b, rno-mir-29c-1, rno-mir-30c-1, rno-mir-30c-2, rno-mir-98, rno-mir-101a, rno-mir-122, rno-mir-126a, rno-mir-130a, rno-mir-133a, rno-mir-142, rno-mir-143, rno-mir-181c, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-194-1, rno-mir-194-2, rno-mir-208a, rno-mir-181a-1, hsa-mir-423, hsa-mir-18b, hsa-mir-20b, hsa-mir-451a, mmu-mir-451a, rno-mir-451, ssc-mir-122, ssc-mir-15b, ssc-mir-181b-2, ssc-mir-19a, ssc-mir-20a, ssc-mir-26a, ssc-mir-326, ssc-mir-181c, ssc-let-7c, ssc-let-7f-1, ssc-let-7i, ssc-mir-18a, ssc-mir-29c, ssc-mir-30c-2, hsa-mir-484, hsa-mir-181d, hsa-mir-499a, rno-mir-1, rno-mir-133b, mmu-mir-484, mmu-mir-20b, rno-mir-20b, rno-mir-378a, rno-mir-499, hsa-mir-378d-2, mmu-mir-423, mmu-mir-499, mmu-mir-181d, mmu-mir-18b, mmu-mir-208b, hsa-mir-208b, rno-mir-17-2, rno-mir-181d, rno-mir-423, rno-mir-484, mmu-mir-1b, ssc-mir-15a, ssc-mir-16-2, ssc-mir-16-1, ssc-mir-17, ssc-mir-130a, ssc-mir-101-1, ssc-mir-101-2, ssc-mir-133a-1, ssc-mir-1, ssc-mir-181a-1, ssc-let-7a-1, ssc-let-7e, ssc-let-7g, ssc-mir-378-1, ssc-mir-133b, ssc-mir-499, ssc-mir-143, ssc-mir-423, ssc-mir-181a-2, ssc-mir-181b-1, ssc-mir-181d, ssc-mir-98, ssc-mir-208b, ssc-mir-142, ssc-mir-19b-1, hsa-mir-378b, ssc-mir-22, rno-mir-126b, rno-mir-208b, rno-mir-133c, hsa-mir-378c, ssc-mir-194b, ssc-mir-133a-2, ssc-mir-484, ssc-mir-30c-1, ssc-mir-126, ssc-mir-378-2, ssc-mir-451, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, mmu-mir-378b, mmu-mir-101c, hsa-mir-451b, hsa-mir-499b, ssc-let-7a-2, ssc-mir-18b, hsa-mir-378j, rno-mir-378b, mmu-mir-133c, mmu-let-7j, mmu-mir-378c, mmu-mir-378d, mmu-mir-451b, ssc-let-7d, ssc-let-7f-2, ssc-mir-20b-1, ssc-mir-20b-2, ssc-mir-194a, mmu-let-7k, mmu-mir-126b, mmu-mir-142b, rno-let-7g, rno-mir-15a, ssc-mir-378b, rno-mir-29c-2, rno-mir-1b, ssc-mir-26b
let-7, miR-98, miR-130a and miR-16 showed uniform levels of expression in 13 different tissues but were hardly detected in pancreas (Figure 3A). [score:3]
Similarly, let-7, miR-98, miR-16 and miR-130a are abundantly expressed in 13 of the 14 tissues (except in pancreas) (Figure 3A). [score:3]
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[+] score: 5
All the five candidate signature miRNAs (miR-29b, miR-31, miR-101a, miR-130a, miR-199a-5p) have been reported to show altered expression levels in different types of cancers (49– 58). [score:3]
MiR-130a also targets dicer1 (68). [score:2]
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A similar selective inhibition of lung tumors was observed in MCS-exposed female Swiss H mice [21], in which 3 miRNAs (miR-10a, miR-125, and miR-130a) involved in estrogen and HER2 pathways were differentially expressed in adenoma-bearing male and female mice [27]. [score:5]
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To validate miRNA targets, approximately 10 [5] 293T cells per well in a 24-well plate were transiently transfected with 0.3μg of each firefly luciferase reporter construct, 0.1μg of Renilla luciferase TK vector, and 0.6μg of pMSCV-miR-128-2 or control vector of pMSCV-miR-130 or pMSCV-miR-29b2. [score:3]
Plasmids encoding miR-130 or miR-29b2 preserved in our laboratory were used as controls. [score:1]
The plasmids pMSCV_GW_RfA_PGK_EGFP-miR-128-2, pMSCV_GW_RfA_PGK_EGFP-miR-130, and pMSCV_GW_RfA_PGK_EGFP-miR-29b2 (hereafter called pMSCV-miR-128-2, pMSCV-miR-130, and pMSCV-miR-29b2, respectively) encoding mature miR-128-2, miR-130, and miR-29b2, respectively, were provided by Dr. [score:1]
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Relevant to polyQ-ATXN1 cytotoxicity, Lee et al. found that ATXN1 levels might be post-transcriptionally regulated by miRNA, specifically miR-19, miR-101, and miR-130. [score:2]
miR-19, miR-101 and miR-130 co-regulate ATXN1 levels to potentially modulate SCA1 pathogenesis. [score:2]
When miR-19, miR101, and miR130 were transfected into HEK293T, HeLa and MCF7 cells, a marked decrease in ATXN1 levels was observed. [score:1]
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miR-130a +Expression of miR-130a was significantly up-regulated in primary glioblastomas compared with normal peripheral brain tissue [44]. [score:5]
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[+] score: 5
Other miRNAs from this paper: mmu-mir-15b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-186, mmu-mir-200b, mmu-mir-202, mmu-mir-30e, mmu-let-7d, mmu-mir-130b, mmu-mir-19b-2, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-192, mmu-mir-200a, mmu-mir-15a, mmu-mir-21a, mmu-mir-29a, mmu-mir-29c, mmu-mir-93, mmu-mir-19a, mmu-mir-200c, mmu-mir-29b-2, mmu-mir-19b-1, mmu-mir-466a, mmu-mir-467a-1, mmu-mir-669a-1, mmu-mir-669b, mmu-mir-669a-2, mmu-mir-669a-3, mmu-mir-467b, mmu-mir-669c, mmu-mir-709, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, mmu-mir-466c-1, mmu-mir-466e, mmu-mir-466f-1, mmu-mir-466f-2, mmu-mir-466f-3, mmu-mir-466g, mmu-mir-466h, mmu-mir-467c, mmu-mir-467d, mmu-mir-574, mmu-mir-466d, mmu-mir-467e, mmu-mir-466l, mmu-mir-669k, mmu-mir-669g, mmu-mir-669d, mmu-mir-466i, mmu-mir-669j, mmu-mir-669f, mmu-mir-669i, mmu-mir-669h, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-467f, mmu-mir-466j, mmu-mir-669e, mmu-mir-467g, mmu-mir-467h, mmu-mir-669l, mmu-mir-669m-1, mmu-mir-669m-2, mmu-mir-669o, mmu-mir-669n, mmu-mir-466m, mmu-mir-669d-2, mmu-mir-466o, mmu-mir-467a-2, mmu-mir-669a-4, mmu-mir-669a-5, mmu-mir-467a-3, mmu-mir-466c-2, mmu-mir-669a-6, mmu-mir-467a-4, mmu-mir-466b-4, mmu-mir-669a-7, mmu-mir-467a-5, mmu-mir-466b-5, mmu-mir-669p-1, mmu-mir-467a-6, mmu-mir-669a-8, mmu-mir-466b-6, mmu-mir-669a-9, mmu-mir-467a-7, mmu-mir-466b-7, mmu-mir-669p-2, mmu-mir-467a-8, mmu-mir-669a-10, mmu-mir-467a-9, mmu-mir-669a-11, mmu-mir-467a-10, mmu-mir-669a-12, mmu-mir-466p, mmu-mir-466n, mmu-mir-466b-8, mmu-mir-466q, mmu-mir-21b, mmu-mir-130c, mmu-mir-21c, mmu-mir-30f, mmu-mir-466c-3
Also, several microRNAs, such as miR-130, miR-192 and miR-200, have been reported to have a regulatory role in kidney diseases [16, 17]. [score:4]
In addition, let-7d-3p [20], miR-21[21], miR-29 [22], miR-30 [23], miR-130 [16], miR-192 [24], miR-200 [25, 26] have been reported to be related to kidney fibrosis. [score:1]
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Specifically, in TNFα -treated adipocytes, miR-146b, miR-130 and miR-155 were upregulated. [score:4]
Several miRNAs, such as miR-132 [15], miR-155 [16], miR-130 [17], miR-145 [18], miR-146b [19], and miR-29 [20] have been indentified in obesity -associated inflammation and insulin-resistance in adipocytes. [score:1]
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[+] score: 5
Other miRNAs from this paper: hsa-mir-16-1, hsa-mir-17, hsa-mir-20a, hsa-mir-21, hsa-mir-23a, hsa-mir-100, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-107, hsa-mir-16-2, mmu-mir-1a-1, mmu-mir-23b, mmu-mir-125b-2, mmu-mir-9-2, mmu-mir-145a, mmu-mir-181a-2, mmu-mir-184, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-205, mmu-mir-206, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-199a-2, hsa-mir-205, hsa-mir-181a-1, hsa-mir-214, hsa-mir-219a-1, hsa-mir-223, mmu-mir-302a, hsa-mir-1-2, hsa-mir-23b, hsa-mir-125b-1, hsa-mir-130a, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125b-2, hsa-mir-184, hsa-mir-206, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-20a, mmu-mir-21a, mmu-mir-23a, mmu-mir-103-1, mmu-mir-103-2, rno-mir-338, mmu-mir-338, rno-mir-20a, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-181b-2, mmu-mir-107, mmu-mir-17, mmu-mir-100, mmu-mir-181a-1, mmu-mir-214, mmu-mir-219a-1, mmu-mir-223, mmu-mir-199a-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-181b-1, mmu-mir-125b-1, hsa-mir-302a, hsa-mir-219a-2, mmu-mir-219a-2, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-367, hsa-mir-372, hsa-mir-338, mmu-mir-181b-2, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-16, rno-mir-17-1, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-100, rno-mir-103-2, rno-mir-103-1, rno-mir-107, rno-mir-125b-1, rno-mir-125b-2, rno-mir-130a, rno-mir-145, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-184, rno-mir-199a, rno-mir-205, rno-mir-206, rno-mir-181a-1, rno-mir-214, rno-mir-219a-1, rno-mir-219a-2, rno-mir-223, hsa-mir-512-1, hsa-mir-512-2, rno-mir-1, mmu-mir-367, mmu-mir-302b, mmu-mir-302c, mmu-mir-302d, rno-mir-17-2, hsa-mir-1183, mmu-mir-1b, hsa-mir-302e, hsa-mir-302f, hsa-mir-103b-1, hsa-mir-103b-2, rno-mir-9b-3, rno-mir-9b-1, rno-mir-9b-2, rno-mir-219b, hsa-mir-23c, hsa-mir-219b, mmu-mir-145b, mmu-mir-21b, mmu-mir-21c, mmu-mir-219b, mmu-mir-219c, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
From the top twenty miRNAs showing highest expression in A2B5+ GalC− cells, miR-130a, miR-16, miR-17, and miR-20a were also in the top twenty expressed miRNAs from our GPs. [score:5]
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This key circulating miRNA signature consists of ten miRNAs (let-7c, let-7b, miR-15a, miR-18a, miR-27a, miR-155, miR-24, miR-130a, miR-10b, and miR-497), which were responsible for DLBCL initiation and was present prior to the formation of visible tumor. [score:1]
The following miRNAs were categorized as oncomiRs for DLBCL: miR-10b [44], miR-155 [9, 19, 29, 44], let-7b [31, 42], miR-18a [1, 14, 41, 44], and miR-130a [44, 46]. [score:1]
Since miRNAs can have different aliases, the 10 miRNAs (Fig 1) are identified as the following for the rest of this manuscript: let-7 = let-7b, let-7a-5p = let-7c, miR-10 = miR-10b, miR-130 = miR-130a, miR-155 = miR-155, miR-27 = miR27a, miR-24-3p = miR-24, miR-17 = miR-18a, miR-15 = miR-15a, and miR-16-5p = miR-497. [score:1]
This miRNA signature consists of 10 miRNAs: miR-130, miR-27, miR-17, miR-10, miR-155, let-7a-5p, let-7, miR-24-3p, miR-15, and miR-16-5p. [score:1]
Five out of the ten miRNAs (let-7c, miR-15a, miR-18a, miR-24, and miR-130a) showed an increased amount of circulating miRNA with age for both Smurf2 [T/T] and wild-type mice (Fig 4). [score:1]
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[+] score: 5
A group of 39 miRNAs was significantly down-regulated by Nkx2-1 knock-down including miR-1195 (−4.9 fold), miR-378 (−4.6 fold), miR-449a (−2.1 fold), and miR-130a (−1.9 fold) (Figure  2A and Table  1). [score:5]
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The majority of the miRNAs had alterations in expression that were consistent between the two species, except for miR-323-3p, miR-369-5p, miR-410, miR-411, miR-433, miR-494 and miR-130a, which were expressed discordantly in the tumors from the two different species (Table 1). [score:5]
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[+] score: 4
In this context, a previous study that grouped together LNCaP, DU145 and PC3 cells identified downregulation of miR-130a, -203, -205 as a signature of castrate-resistant and metastatic prostate cancer [46]. [score:4]
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By performing microarray screening on exosomes, we found nine inflammatory miRNAs which were deregulated in sera of chronic alcohol-fed mice compared to controls including upregulated miRNAs: miRNA-192, miRNA-122, miRNA-30a, miRNA-744, miRNA-1246, miRNA 30b and miRNA-130a. [score:4]
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This could explain why miR-15b and miR-130 (down-regulated in HCC tissues in contrast to miR-15b) could be used as a set of highly accurate markers for HBV-related HCC (16). [score:4]
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49
[+] score: 4
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-20a, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-29a, hsa-mir-30a, hsa-mir-93, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-107, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-15b, mmu-mir-23b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-101a, mmu-mir-124-3, mmu-mir-125a, mmu-mir-9-2, mmu-mir-135a-1, mmu-mir-136, mmu-mir-138-2, mmu-mir-140, mmu-mir-144, mmu-mir-145a, mmu-mir-146a, mmu-mir-149, mmu-mir-152, mmu-mir-10b, mmu-mir-181a-2, mmu-mir-182, mmu-mir-183, mmu-mir-185, mmu-mir-24-1, mmu-mir-191, mmu-mir-193a, mmu-mir-195a, mmu-mir-200b, mmu-mir-204, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10a, hsa-mir-10b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-183, hsa-mir-204, hsa-mir-181a-1, hsa-mir-221, hsa-mir-222, hsa-mir-200b, mmu-mir-301a, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, mmu-mir-130b, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-30b, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-130a, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-138-2, hsa-mir-140, hsa-mir-144, hsa-mir-145, hsa-mir-152, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-136, hsa-mir-138-1, hsa-mir-146a, hsa-mir-149, hsa-mir-185, hsa-mir-193a, hsa-mir-195, hsa-mir-320a, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-20a, mmu-mir-23a, mmu-mir-24-2, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-93, mmu-mir-34a, mmu-mir-330, mmu-mir-339, mmu-mir-340, mmu-mir-135b, mmu-mir-101b, hsa-mir-200c, hsa-mir-181b-2, mmu-mir-107, mmu-mir-10a, mmu-mir-17, mmu-mir-200c, mmu-mir-181a-1, mmu-mir-320, mmu-mir-26a-2, mmu-mir-221, mmu-mir-222, mmu-mir-29b-2, mmu-mir-135a-2, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-181c, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-101-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-301a, hsa-mir-130b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-361, mmu-mir-361, hsa-mir-376a-1, mmu-mir-376a, hsa-mir-340, hsa-mir-330, hsa-mir-135b, hsa-mir-339, hsa-mir-335, mmu-mir-335, mmu-mir-181b-2, mmu-mir-376b, mmu-mir-434, mmu-mir-467a-1, hsa-mir-376b, hsa-mir-485, hsa-mir-146b, hsa-mir-193b, hsa-mir-181d, mmu-mir-485, mmu-mir-541, hsa-mir-376a-2, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, mmu-mir-301b, mmu-mir-674, mmu-mir-146b, mmu-mir-467b, mmu-mir-669c, mmu-mir-708, mmu-mir-676, mmu-mir-181d, mmu-mir-193b, mmu-mir-467c, mmu-mir-467d, hsa-mir-541, hsa-mir-708, hsa-mir-301b, mmu-mir-467e, mmu-mir-467f, mmu-mir-467g, mmu-mir-467h, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, mmu-mir-467a-2, mmu-mir-467a-3, mmu-mir-467a-4, mmu-mir-467a-5, mmu-mir-467a-6, mmu-mir-467a-7, mmu-mir-467a-8, mmu-mir-467a-9, mmu-mir-467a-10, hsa-mir-320e, hsa-mir-676, mmu-mir-101c, mmu-mir-195b, mmu-mir-145b, mmu-let-7j, mmu-mir-130c, mmu-mir-30f, mmu-let-7k, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
The miRNA families that change expression in both mice and rats were: mir-7, mir-9, mir-10, mir-15, mir-17, mir-26, mir-29, mir-30, mir-101, mir-130, mir-181, mir-204, mir-339, mir-340, mir-368, mir-434, mir-467. [score:3]
26E-0212mmu-miR-101b-3pmir-1010.297.791.72E-059.11E-0437mmu-miR-101a-3pmir-1010.2410.121.17E-031.92E-0250mmu-miR-107-3pmir-1030.228.773.24E-034.12E-0264mmu-miR-124-5pmir-1240.156.327.13E-037.09E-0233mmu-miR-301a-3pmir-1300.228.396.90E-041.29E-0259mmu-miR-130a-3pmir-1300.168.305.94E-036.44E-0252mmu-miR-135b-5pmir-1350.227.924.08E-034.99E-0274mmu-miR-136-5pmir-1360.229.061.09E-029. [score:1]
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50
[+] score: 4
uL5 (rpL11) directly binds to c-Myc MBII domain [53] but also recruits of micro -RNA -induced silencing complex (miRISC) with miR-24 or miR-130a to c-Myc mRNA at its 3′ untranslated region (3′-UTR), leading to c-Myc mRNA degradation [54]. [score:4]
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51
[+] score: 4
They observed enhanced levels of miR-21 and miR-130 in venous ulcers patients, which delay healing of human wounds by targeting leptin receptor (LepR) [13]. [score:3]
Some notable examples include miR-130a, miR-132, miR-155, miR-198, miR-21, miR-31 and miR-378a 13, 23, 24, 26, 28– 30. miR-155 acts as an important player in controlling the inflammatory response during skin repair; genetic deletion of miR-155 in mice leads to accelerated healing associated with elevated numbers of macrophages and increased type-1 collagen deposition in wounded tissue [30]. [score:1]
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52
[+] score: 4
Additional data indicate that FGF and BMP signaling pathway interactions are regulated by negative feedback loops involving microRNAs, particularly miR-130 and miR-133 [48, 49]. [score:2]
Lopez-Sanchez C. Franco D. Bonet F. Garcia-Lopez V. Aranega A. Garcia-Martinez V. Negative fgf8-bmp2 feed-back is regulated by mir-130 during early cardiac specification Dev. [score:2]
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53
[+] score: 4
A recent study has demonstrated that miR-130 family negatively regulates PTEN protein expression in bladder cancer cells 34. [score:4]
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54
[+] score: 4
E14.5) microRNA 205; RIKEN cDNA 4631405K08 gene Mir205 - - -2.38 microRNA 669d Mir669d - - -2.07 glutamate-ammonia ligase (glutamine synthetase); microRNA 8114 Glul - - 2.14 microRNA 130a Mir130a - - 2.28miRNAs reported as downregulated in ageing skeletal muscle are written in bold text [39]. [score:4]
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55
[+] score: 4
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-26b, hsa-mir-29a, hsa-mir-30a, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, mmu-let-7g, mmu-let-7i, mmu-mir-15b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-138-2, mmu-mir-181a-2, mmu-mir-182, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-10a, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-181a-1, mmu-mir-297a-1, mmu-mir-297a-2, mmu-mir-301a, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, mmu-mir-106a, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-130a, hsa-mir-138-2, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-138-1, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-34a, rno-mir-301a, rno-let-7d, rno-mir-344a-1, mmu-mir-344-1, rno-mir-346, mmu-mir-346, rno-mir-352, hsa-mir-181b-2, mmu-mir-10a, mmu-mir-181a-1, mmu-mir-29b-2, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-181c, mmu-mir-125b-1, hsa-mir-106b, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-34b, hsa-mir-34c, hsa-mir-301a, hsa-mir-30e, hsa-mir-362, mmu-mir-362, hsa-mir-369, hsa-mir-374a, mmu-mir-181b-2, hsa-mir-346, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-10a, rno-mir-15b, rno-mir-26b, rno-mir-29b-2, rno-mir-29a, rno-mir-29b-1, rno-mir-29c-1, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-34b, rno-mir-34c, rno-mir-34a, rno-mir-106b, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-130a, rno-mir-138-2, rno-mir-138-1, rno-mir-181c, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-181a-1, hsa-mir-449a, mmu-mir-449a, rno-mir-449a, mmu-mir-463, mmu-mir-466a, hsa-mir-483, hsa-mir-493, hsa-mir-181d, hsa-mir-499a, hsa-mir-504, mmu-mir-483, rno-mir-483, mmu-mir-369, rno-mir-493, rno-mir-369, rno-mir-374, hsa-mir-579, hsa-mir-582, hsa-mir-615, hsa-mir-652, hsa-mir-449b, rno-mir-499, hsa-mir-767, hsa-mir-449c, hsa-mir-762, mmu-mir-301b, mmu-mir-374b, mmu-mir-762, mmu-mir-344d-3, mmu-mir-344d-1, mmu-mir-673, mmu-mir-344d-2, mmu-mir-449c, mmu-mir-692-1, mmu-mir-692-2, mmu-mir-669b, mmu-mir-499, mmu-mir-652, mmu-mir-615, mmu-mir-804, mmu-mir-181d, mmu-mir-879, mmu-mir-297a-3, mmu-mir-297a-4, mmu-mir-344-2, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, mmu-mir-466c-1, mmu-mir-466e, mmu-mir-466f-1, mmu-mir-466f-2, mmu-mir-466f-3, mmu-mir-466g, mmu-mir-466h, mmu-mir-493, mmu-mir-504, mmu-mir-466d, mmu-mir-449b, hsa-mir-374b, hsa-mir-301b, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-879, mmu-mir-582, rno-mir-181d, rno-mir-182, rno-mir-301b, rno-mir-463, rno-mir-673, rno-mir-652, mmu-mir-466l, mmu-mir-669k, mmu-mir-466i, mmu-mir-669i, mmu-mir-669h, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-466j, mmu-mir-1193, mmu-mir-767, rno-mir-362, rno-mir-504, rno-mir-582, rno-mir-615, mmu-mir-3080, mmu-mir-466m, mmu-mir-466o, mmu-mir-466c-2, mmu-mir-466b-4, mmu-mir-466b-5, mmu-mir-466b-6, mmu-mir-466b-7, mmu-mir-466p, mmu-mir-466n, mmu-mir-344e, mmu-mir-344b, mmu-mir-344c, mmu-mir-344g, mmu-mir-344f, mmu-mir-374c, mmu-mir-466b-8, hsa-mir-466, hsa-mir-1193, rno-mir-449c, rno-mir-344b-2, rno-mir-466d, rno-mir-344a-2, rno-mir-1193, rno-mir-344b-1, hsa-mir-374c, hsa-mir-499b, mmu-mir-466q, mmu-mir-344h-1, mmu-mir-344h-2, mmu-mir-344i, rno-mir-344i, rno-mir-344g, mmu-let-7j, mmu-mir-30f, mmu-let-7k, mmu-mir-692-3, rno-let-7g, rno-mir-15a, rno-mir-762, mmu-mir-466c-3, rno-mir-29c-2, rno-mir-29b-3, rno-mir-344b-3, rno-mir-466b-3, rno-mir-466b-4
Our study showed that no miRNA was different between males and females in adenoma-free mice, while 3 miRNAs (miR-10a, miR-125, and miR-130a) were differentially expressed in adenoma-bearing male and female mice. [score:3]
In particular, miR-10a is related to estrogen dependent cancer promotion [112, 113], miR-130a both to the estrogen and HER2 pathways [114, 115], and miR-125 to HER2/erbb2 estrogen sensitive oncogene activation [116, 117]. [score:1]
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56
[+] score: 3
Analysis of miR-4295, miR-301a, miR-301b, miR-130a, miR-130b, miR-454, and miR-3666 expression were carried out using the miScript PCR system (QIAGEN, Valencia, CA) by 7900HT Fast Real-time PCR system (Applied Biosystems, Foster City, CA). [score:3]
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57
[+] score: 3
Three miRNAs associated with human basal-type tumors (miR-135b, miR-505 and miR-155), and seven miRNAs associated with human luminal type tumors (let-7a, let-7f, miR-100, miR-130a, miR-152, miR-214 and miR-29b) are similarly expressed in mouse basal-like and luminal-type tumors, respectively. [score:3]
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58
[+] score: 3
Specific miRNAs that enhance adipocyte differentiation (miR-30c, miR-143, miR-146b, and miR-378; [21– 24]) or inhibit adipocyte differentiation (miR-27, miR-130, and miR-138; [25– 27]) have been identified. [score:3]
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59
[+] score: 3
Egawa H Jingushi K Hirono T Ueda Y Kitae K Nakata W Fujita K Uemura M Nonomura N Tsujikawa K The miR-130 family promotes cell migration and invasion in bladder cancer through FAK and Akt phosphorylation by regulating PTENSci Rep. [score:2]
A recent study has identified microRNA-130 (miR-130) as a contributor in mesenchymal differentiation, hypoxic response modulation and tumorigenesis in colorectal cancer [5]. [score:1]
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60
[+] score: 3
Other miRNAs from this paper: mmu-mir-146a, hsa-mir-130a, hsa-mir-146a, hsa-mir-146b, mmu-mir-146b
Wang Y MiR-130a-3p attenuates activation and induces apoptosis of hepatic stellate cells in nonalcoholic fibrosing steatohepatitis by directly targeting TGFBR1 and TGFBR2Cell Death Dis. [score:3]
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61
[+] score: 3
Our screen identified five miRNAs, miR-130a-3p, miR-125b-5p, miR-29c-3p, miR-16-5p and miR-23b-3p, whose mimics suppressed FAS -induced apoptosis in primary hepatocytes (Fig. 1h). [score:3]
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62
[+] score: 3
The expression of miR-130a-3p and miR-106a/b-5p were too low to be detected in tTreg cells, while miR-17-5p and miR-20b-5p showed no change in the process of expansion (data not shown). [score:3]
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63
[+] score: 3
Elevated miR-130a/miR130b/miR-152 expression reduces intracellular ATP levels in the pancreatic beta cell. [score:3]
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64
[+] score: 2
Up to now, there have been very few miRNAs, such as miR-130a-3p[41], miR-26a[42] and miR-155 (this study), to be found to act as positive regulators of glucose tolerance and insulin sensitivity in vivo. [score:2]
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65
[+] score: 2
A few miRNAs, like miR-30a, miR-101, miR-376b, miR-130a, miR-375, miR-502, have been identified as the regulators of autophagy [6- 9]. [score:2]
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66
[+] score: 2
To date, only one study has addressed a role for microRNA in vascular development during branching morphogenesis of the lung, where miR-221 and miR-130a appear to have opposing effects on tube formation and migration of mouse foetal lung endothelial cells [25]. [score:2]
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67
[+] score: 2
miR-19, miR-101 and miR-130 co-regulate ATXN1 levels to potentially modulate SCA1 pathogenesis. [score:2]
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68
[+] score: 2
For instance, miR-142-5p plays critical roles in lymphocyte development and homeostasis (57), and miR-106a-5p, miR-130-3p, miR-20b-5p, miR-345-3p, and the miR-15 cluster have been associated with immune or stress responses (58– 62). [score:2]
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69
[+] score: 2
Among these 17 dynamically regulated miRNAs, the top 5 with the greatest fold change were miR-126 (23-fold), miR-34c (17-fold), miR-130a (12-fold), miR-574 (9-fold) and miR-193b (8-fold). [score:2]
[1 to 20 of 1 sentences]
70
[+] score: 2
miR-142-5p and miR130a-3p are regulated by IL-4 and Il-13 and control profibrogenic macrophage program. [score:2]
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71
[+] score: 2
Mmu-miR-130a-3p (2 targets), Meox2 [Western blot &], Zfpm2 [Luciferase reporter assay//Northern blot//Western blot]. [score:2]
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72
[+] score: 2
Expression of 18s rRNA, primary miR-29a, mature miR-29a/b/c, miR-122 and miR-130a was assessed using individual Taqman assays (Applied Biosystems). [score:2]
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73
[+] score: 2
We selected 14 of these miRs which might have been involved in regulation of angiogenesis, including miR-17-5p, miR-19a, miR-23a, miR-24, miR-31, miR-34a, miR-126, miR-130a, miR-132, miR-16, miR-21, miR-217, miR-221, and miR-378 for our study. [score:2]
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74
[+] score: 2
This analysis indicated miR-27a/b, miR-130a/b, miR-301a/b, and miR-454 as potential regulators of PPARγ. [score:2]
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75
[+] score: 2
Other miRNAs from this paper: mmu-mir-142a, mmu-mir-21a, mmu-mir-21b, mmu-mir-21c, mmu-mir-142b
miR-142-5p and miR-130a-3p are regulated by IL-4 and IL-13 and control profibrogenic macrophage program. [score:2]
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76
[+] score: 1
As shown in Figure 5D, miRNAs miR-19a, miR-21, miR-27a, miR-130 and miR-146a were enriched within exosomes and virtually undetectable as free, circulating miRNAs in the supernatant. [score:1]
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77
[+] score: 1
P <0.01 for miR-17, 18a, 19b-1, 20a, 92a-1 and 210, P < 0.05 for miR-19a, 126 and 296 and P > 0.05 for miR-130. [score:1]
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78
[+] score: 1
These include miR21, miR200 family, miR34 family, miR130a, miR203, miR19a and miR205. [score:1]
[1 to 20 of 1 sentences]
79
[+] score: 1
Other miRNAs from this paper: hsa-let-7a-2, hsa-let-7c, hsa-let-7e, hsa-mir-15a, hsa-mir-16-1, hsa-mir-21, hsa-mir-22, hsa-mir-23a, hsa-mir-24-2, hsa-mir-100, hsa-mir-29b-2, mmu-let-7i, mmu-mir-99b, mmu-mir-125a, mmu-mir-142a, mmu-mir-144, mmu-mir-155, mmu-mir-183, hsa-mir-196a-1, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, hsa-mir-148a, mmu-mir-143, hsa-mir-181c, hsa-mir-183, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-181a-1, hsa-mir-200b, mmu-mir-298, mmu-mir-34b, hsa-let-7i, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-130a, hsa-mir-142, hsa-mir-143, hsa-mir-144, hsa-mir-125a, mmu-mir-148a, mmu-mir-196a-1, mmu-let-7a-2, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-mir-15a, mmu-mir-16-1, mmu-mir-21a, mmu-mir-22, mmu-mir-23a, mmu-mir-24-2, rno-mir-148b, mmu-mir-148b, hsa-mir-200c, hsa-mir-155, mmu-mir-100, mmu-mir-200c, mmu-mir-181a-1, mmu-mir-29b-2, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-181c, hsa-mir-34b, hsa-mir-99b, hsa-mir-374a, hsa-mir-148b, rno-let-7a-2, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7i, rno-mir-21, rno-mir-22, rno-mir-23a, rno-mir-24-2, rno-mir-29b-2, rno-mir-34b, rno-mir-99b, rno-mir-100, rno-mir-124-1, rno-mir-124-2, rno-mir-125a, rno-mir-130a, rno-mir-142, rno-mir-143, rno-mir-144, rno-mir-181c, rno-mir-183, rno-mir-199a, rno-mir-200c, rno-mir-200b, rno-mir-181a-1, rno-mir-298, hsa-mir-193b, hsa-mir-497, hsa-mir-568, hsa-mir-572, hsa-mir-596, hsa-mir-612, rno-mir-664-1, rno-mir-664-2, rno-mir-497, mmu-mir-374b, mmu-mir-497a, mmu-mir-193b, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-568, hsa-mir-298, hsa-mir-374b, rno-mir-466b-1, rno-mir-466b-2, hsa-mir-664a, mmu-mir-664, rno-mir-568, hsa-mir-664b, mmu-mir-21b, mmu-mir-21c, rno-mir-155, mmu-mir-142b, mmu-mir-497b, rno-mir-148a, rno-mir-15a, rno-mir-193b
A few pri-miRNAs exhibit conservation along the entire length of the pri-miRNA (for example mir-497~195, mir-99b~let-7c~mir-125a, mir-124-2, mir-130a and mmu-mir-568) (Figure 10). [score:1]
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The C-terminal NHL domain of TRIM-32 forms complex with Ago1, and thereby promotes the efficiency of processing of a number of miRNAs [Figure 2], including let-7, miR-134, miR-130, miR-214, 449, 379, 181, and miR-503 [31]. [score:1]
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miR-130 has been shown to strongly reduce adipogenesis by repressing PPAR-γ biosynthesis in human primary preadipocytes and 3T3-L1 mouse adipocytes [17]. [score:1]
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82
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PCR analysis was performed using cDNA in triplicate on the 7900 HT Fast Realtime system (Applied Biosystems) for the following primary-miRNA transcripts using Applied Biosystems pri-miRNA gui delines; pri-mir181d (Hs03303910_pri), pri-mir130a (Hs03303108_pri), pri-let7d (Hs03302562_pri) and pri-mir23b (Hs03303058_pri). [score:1]
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83
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Among the differentially expressed microRNAs were miR-181a, miR-208-5p or miR-499, miR-130a, miR-26a and miR-30c with previously characterised functions in skeletal muscle. [score:1]
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84
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The remaining pri-miRNAs did not increase in response to p-Smad2/3 induction, with one pri-miRNA (pri-miR-130a) responding to CHX (Figure 2B). [score:1]
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85
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It is reported that exosomes contain plenty of miRs, including pro-angiomiRs (miR-21, miR-126, miR-130a, miR-132, miR-210, miR-378 and let-7f, etc. ) [score:1]
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These include mir-24-2, mir-30c-2, mir-125a, mir-130a, mir-196, mir-215, mir-218-2, and mir-367. [score:1]
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87
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Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-32, hsa-mir-33a, hsa-mir-99a, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-107, mmu-let-7g, mmu-let-7i, mmu-mir-15b, mmu-mir-99a, mmu-mir-126a, mmu-mir-128-1, mmu-mir-140, mmu-mir-154, mmu-mir-204, mmu-mir-143, hsa-mir-204, hsa-mir-211, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-222, hsa-mir-223, mmu-mir-301a, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-128-1, hsa-mir-130a, hsa-mir-140, hsa-mir-143, hsa-mir-126, hsa-mir-129-2, hsa-mir-154, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-27a, mmu-mir-129-2, mmu-mir-103-1, mmu-mir-103-2, mmu-mir-340, mmu-mir-107, mmu-mir-32, mmu-mir-218-1, mmu-mir-218-2, mmu-mir-223, mmu-mir-26a-2, mmu-mir-211, mmu-mir-222, mmu-mir-128-2, hsa-mir-128-2, hsa-mir-29c, hsa-mir-101-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-301a, hsa-mir-26a-2, hsa-mir-379, mmu-mir-379, hsa-mir-340, mmu-mir-409, hsa-mir-409, hsa-mir-499a, hsa-mir-455, hsa-mir-670, mmu-mir-1249, mmu-mir-670, mmu-mir-499, mmu-mir-455, bta-mir-26a-2, bta-mir-29a, bta-let-7f-2, bta-mir-101-2, bta-mir-103-1, bta-mir-16b, bta-mir-222, bta-mir-26b, bta-mir-27a, bta-mir-499, bta-mir-99a, bta-mir-126, bta-mir-128-1, bta-mir-34b, bta-mir-107, bta-mir-140, bta-mir-15b, bta-mir-218-2, bta-let-7d, bta-mir-29c, bta-mir-455, bta-let-7g, bta-let-7a-1, bta-let-7f-1, bta-let-7i, bta-mir-34c, bta-let-7a-2, bta-let-7a-3, bta-let-7b, bta-let-7c, bta-let-7e, bta-mir-103-2, bta-mir-204, hsa-mir-1249, hsa-mir-1306, hsa-mir-103b-1, hsa-mir-103b-2, bta-mir-128-2, bta-mir-129-2, bta-mir-130a, bta-mir-143, bta-mir-154a, bta-mir-211, bta-mir-218-1, bta-mir-223, bta-mir-26a-1, bta-mir-301a, bta-mir-32, bta-mir-33a, bta-mir-340, bta-mir-379, bta-mir-409a, bta-mir-670, mmu-mir-1306, bta-mir-1306, bta-mir-1249, bta-mir-2284i, bta-mir-2285a, bta-mir-2284s, bta-mir-2285d, bta-mir-2284l, bta-mir-2284j, bta-mir-2284t, bta-mir-2285b-1, bta-mir-2284d, bta-mir-2284n, bta-mir-2284g, bta-mir-2284p, bta-mir-2284u, bta-mir-2284f, bta-mir-2284a, bta-mir-2284k, bta-mir-2284c, bta-mir-2284v, bta-mir-2285c, bta-mir-2284q, bta-mir-2284m, bta-mir-2284b, bta-mir-2284r, bta-mir-2284h, bta-mir-2284o, bta-mir-2284e, hsa-mir-1260b, bta-mir-2284w, bta-mir-2284x, bta-mir-409b, hsa-mir-499b, bta-mir-1260b, bta-mir-2284y-1, bta-mir-2285e-1, bta-mir-2285e-2, bta-mir-2285f-1, bta-mir-2285f-2, bta-mir-2285g-1, bta-mir-2285h, bta-mir-2285i, bta-mir-2285j-1, bta-mir-2285j-2, bta-mir-2285k-1, bta-mir-2285l, bta-mir-6119, mmu-let-7j, bta-mir-2285o-1, bta-mir-2285o-2, bta-mir-2285n-1, bta-mir-2285n-2, bta-mir-2285p, bta-mir-2285m-1, bta-mir-2285m-2, bta-mir-2284y-2, bta-mir-2285n-3, bta-mir-2285n-4, bta-mir-2284y-3, bta-mir-154c, bta-mir-154b, bta-mir-2285o-3, bta-mir-2285o-4, bta-mir-2285m-3, bta-mir-2284y-4, bta-mir-2284y-5, bta-mir-2284y-6, bta-mir-2285m-4, bta-mir-2285o-5, bta-mir-2285m-5, bta-mir-2285n-5, bta-mir-2285n-6, bta-mir-2284y-7, bta-mir-2285n-7, bta-mir-2284z-1, bta-mir-2284aa-1, bta-mir-2285k-2, bta-mir-2284z-3, bta-mir-2284aa-2, bta-mir-2284aa-3, bta-mir-2285k-3, bta-mir-2285k-4, bta-mir-2284z-4, bta-mir-2285k-5, bta-mir-2284z-5, bta-mir-2284z-6, bta-mir-2284z-7, bta-mir-2284aa-4, bta-mir-2285q, bta-mir-2285r, bta-mir-2285s, bta-mir-2285t, bta-mir-2285b-2, bta-mir-2285v, bta-mir-2284z-2, mmu-let-7k, mmu-mir-126b, bta-mir-2285g-2, bta-mir-2285g-3, bta-mir-2285af-1, bta-mir-2285af-2, bta-mir-2285y, bta-mir-2285w, bta-mir-2285x, bta-mir-2285z, bta-mir-2285u, bta-mir-2285aa, bta-mir-2285ab, bta-mir-2284ab, bta-mir-2285ac, bta-mir-2285ad, bta-mir-2284ac, bta-mir-2285ae, chi-let-7a, chi-let-7b, chi-let-7c, chi-let-7d, chi-let-7e, chi-let-7f, chi-let-7g, chi-let-7i, chi-mir-103, chi-mir-107, chi-mir-1249, chi-mir-126, chi-mir-1306, chi-mir-130a, chi-mir-140, chi-mir-143, chi-mir-154a, chi-mir-154b, chi-mir-15b, chi-mir-16b, chi-mir-204, chi-mir-211, chi-mir-222, chi-mir-223, chi-mir-2284a, chi-mir-2284b, chi-mir-2284c, chi-mir-2284d, chi-mir-2284e, chi-mir-26a, chi-mir-26b, chi-mir-27a, chi-mir-29a, chi-mir-29c, chi-mir-301a, chi-mir-33a, chi-mir-340, chi-mir-34b, chi-mir-34c, chi-mir-379, chi-mir-409, chi-mir-455, chi-mir-499, chi-mir-99a, bta-mir-2285ag, bta-mir-2285ah, bta-mir-2285ai, bta-mir-2285aj, bta-mir-2285ak, bta-mir-2285al, bta-mir-2285am, bta-mir-2285ar, bta-mir-2285as-1, bta-mir-2285as-2, bta-mir-2285as-3, bta-mir-2285at-1, bta-mir-2285at-2, bta-mir-2285at-3, bta-mir-2285at-4, bta-mir-2285au, bta-mir-2285av, bta-mir-2285aw, bta-mir-2285ax-1, bta-mir-2285ax-2, bta-mir-2285ax-3, bta-mir-2285ay, bta-mir-2285az, bta-mir-2285an, bta-mir-2285ao-1, bta-mir-2285ao-2, bta-mir-2285ap, bta-mir-2285ao-3, bta-mir-2285aq-1, bta-mir-2285aq-2, bta-mir-2285ba-1, bta-mir-2285ba-2, bta-mir-2285bb, bta-mir-2285bc, bta-mir-2285bd, bta-mir-2285be, bta-mir-2285bf-1, bta-mir-2285bf-2, bta-mir-2285bf-3, bta-mir-2285bg, bta-mir-2285bh, bta-mir-2285bi-1, bta-mir-2285bi-2, bta-mir-2285bj-1, bta-mir-2285bj-2, bta-mir-2285bk, bta-mir-2285bl, bta-mir-2285bm, bta-mir-2285bn, bta-mir-2285bo, bta-mir-2285bp, bta-mir-2285bq, bta-mir-2285br, bta-mir-2285bs, bta-mir-2285bt, bta-mir-2285bu-1, bta-mir-2285bu-2, bta-mir-2285bv, bta-mir-2285bw, bta-mir-2285bx, bta-mir-2285by, bta-mir-2285bz, bta-mir-2285ca, bta-mir-2285cb, bta-mir-2285cc, bta-mir-2285cd, bta-mir-2285ce, bta-mir-2285cf, bta-mir-2285cg, bta-mir-2285ch, bta-mir-2285ci, bta-mir-2285cj, bta-mir-2285ck, bta-mir-2285cl, bta-mir-2285cm, bta-mir-2285cn, bta-mir-2285co, bta-mir-2285cp, bta-mir-2285cq, bta-mir-2285cr-1, bta-mir-2285cr-2, bta-mir-2285cs, bta-mir-2285ct, bta-mir-2285cu, bta-mir-2285cv-1, bta-mir-2285cv-2, bta-mir-2285cw-1, bta-mir-2285cw-2, bta-mir-2285cx, bta-mir-2285cy, bta-mir-2285cz, bta-mir-2285da, bta-mir-2285db, bta-mir-2285dc, bta-mir-2285dd, bta-mir-2285de, bta-mir-2285df, bta-mir-2285dg, bta-mir-2285dh, bta-mir-2285di, bta-mir-2285dj, bta-mir-2285dk, bta-mir-2285dl-1, bta-mir-2285dl-2, bta-mir-2285dm
The mir-34b/34c cluster, containing mir-34b, mir-34c, mir-670, mir-129-2 and mir-130a, was also identified within QTL regions for milk fat yield and for milk protein yield on BTA 15. [score:1]
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miR-10b, miR-99a, miR-130a, miR-146b, miR-150, and miR-320 were amongst those found to drive Treg differentiation. [score:1]
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Log FC offset P-val (a) P-val (b) hsa-mir-19a Early 125/50.20% −2.485 0.031 1.5023E-05 2.19E-06 hsa-mir-106 Early 156/56.52% −3.929 0.030 2.3594E-05 3.10E-07 hsa-mir-181a Early 125/49.02% −0.242 0.029 0.0001 3.42E-06 miR-93 Early 72/50.35% −3.272 0.030 0.0019 1.78E-05 mmu-mir-153 Early 75/48.08% −0.610 0.036 0.0108 0.0088 hsa-mir-92-1,2 Early 128/55.65% −5.035 0.024 0.0109 0.0001 miR-130 Early 99/57.56% −1. [score:1]
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In addition to miR-122-5p, the miRNA species miR-22, miR-29b, miR-29c, miR-130a and miR-193 were increased in both mice and humans. [score:1]
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