sort by

123 publications mentioning mmu-mir-451b (showing top 100)

Open access articles that are associated with the species Mus musculus and mention the gene name mir-451b. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 168
Other miRNAs from this paper: hsa-mir-451a, mmu-mir-451a, hsa-mir-451b
To determine whether intratumoral miR-451 administration affected the expression of factors in the PI3K/AKT signaling pathway, the expressions of CAB39, LKB1, AMPK, p-AMPK, PI3K and p-AKT were tested and were found to show significant downregulation in an immunohistopathological examination (Fig. 5C). [score:8]
We further analyzed the signaling pathway miR-451 might regulate in human glioma and found that miR-451 modulated the expression of multiple downstream molecules such as LKB1, AMPK, PI3K and AKT, suggesting that miR-451 may act as a tumor-suppressor factor and regulate the PI3K/AKT pathway through LKB1 and AMPK. [score:7]
Consistently, over -expression of miR-451 led to a marked downregulation of factors upstream of AKT. [score:6]
Although the reported under -expression of miR-451 in some types of tumors suggested a role in cancer development, the underlying mechanism is still unclear because little is known about the miR-451 target genes. [score:6]
Consistently, over -expression of miR-451 led to a marked down-regulation of LKB1, AMPK, p-AMPK, and PI3K, all of which are involved in the pathway upstream of AKT (Fig. 4A). [score:6]
miR-451 was down-regulated in glioma tissues and a significant negative correlation was revealed between miR-451 expression and glioma WHO grades. [score:6]
For a second prediction of possible hsa-miR-451 (human miR-451) gene targets we used MicroCosm Targets (http://microrna. [score:5]
However, using the STRING proteins functional association network database, AKT1 was shown to have a direct association with AKTIP and YWHAZ and an indirect association with CAB39, all three of these genes were predicted to be hsa-miR-451 target genes (Fig. 1). [score:5]
These data suggest that the tumor suppressor activity of miR-451 in glioblastoma cells likely acts through its regulation of the PI3K/AKT pathway. [score:4]
Previous data from our laboratory showed that miR-451 had a significant impact on cell proliferation, invasion and apoptosis in human glioblastoma cell lines, possibly by regulating AKT expression (18). [score:4]
Therefore, the identification of miR-451-regulated targets is a necessary step to understand how miR-451 functions. [score:4]
Quantitative real-time PCR showed that miR-451 expression increased in U251, LN229, A172, and U87 cells by 340.14, 849.22, 1680.88 and 2033.85-fold respectively after transfection with the miR-451 mimics, compared to its expression in the control and scramble treated cells (Fig. 3A). [score:4]
It is possible that hsa-miR-451 interacts indirectly with AKT1, through its target genes. [score:4]
The expression of miR-451 decreased markedly in high grade gliomas (WHO grades III and IV) compared to its expression in low grade gliomas (WHO grades I and II). [score:4]
Previously we have shown that miR-451 expression was negatively correlated with glioma WHO grades in quantitative real-time PCR and in situ hybridization. [score:3]
miR-451 inhibited the growth of LN229 glioblastoma cells in vivo. [score:3]
Expressions of mature miR-451 were quantified by miR-qRT PCR using the Hairpin-it™ miRNA qPCR Quantitation kit (GenePharma Co. [score:3]
Previous studies in our laboratory have shown a negative correlation between miR-451 and the expressions of AKT1 and c-Myc (18). [score:3]
miR-451 target gene(s) identification. [score:3]
org) to search for candidate miR-451 target genes and found 14 (YTHDF2, ZNF644, CUGBP2, C11orf30, FMNL3, FBXO33, AKTIP, VAPA, RKHD2, SAMD4B, OSR1, TTN, CAB39, YWHAZ). [score:3]
analysis revealed that miR-451 was expressed in gliomas and its total positive rate was 94.67% (71/75). [score:3]
miR-451 expression was negatively correlated with the WHO grades of gliomas. [score:3]
Increasing the expression of miR-451 might be a useful therapeutic strategy for treating glioma in the future. [score:3]
CAB39 is a target gene of miR-451 in glioma. [score:3]
As shown (Fig. 2A and B), miR-451 expression decreased with the increasing WHO grades of glioma tissues. [score:3]
Together, these data demonstrated that CAB39 is a target gene of the miR-451 in glioma. [score:3]
We used a three-step consequential approach to identify miR-451 target genes. [score:3]
Analysis of hsa-miR-451 candidate target genes. [score:3]
Both the STRING and KEGG databases indicated that CAB39 was the preferential candidate target gene of hsa-miR-451. [score:3]
miR-451 target gene confirmation. [score:3]
The transfected cells were used in subsequent Western blot assays and CAB39 was found to be significantly downregulated in cells treated with the hsa-miR-451 mimic oligonucleotide. [score:3]
In this study, we confirmed the hypo -expression of miR-451 in gliomas using quantitative real-time PCR and fluorescent in situ hybridization. [score:3]
This evidence, both in vitro and in vivo, implied that miR-451 can suppress cell proliferation in human glioma through the LKB1/AMPK and PI3K/AKT pathway. [score:3]
de/STRING/) (19), to explore possible interactions between the 14 candidate miR-451 target genes and AKT1 and c-Myc. [score:3]
Studies have shown that miR-451 inhibited cell growth (3), proliferation, and invasion and enhance apoptosis (18). [score:3]
Bioinformatics analysis failed to identify AKT1 and/or c-Myc as hsa-miR-451 target genes. [score:3]
To further study the biological role of miR-451 in human glioma tissues, we examined miR-451 expression in normal brain tissues, glioma tissues and glioma cell lines by quantitative RT-PCR. [score:3]
To exploit the possible interactions that were identified between the miR-451 target genes and AKT1 and c-Myc we used the KEGG pathway database (http://www. [score:3]
The calcium binding protein 39 gene (CAB39) predicted by bioinformatics analysis as a target gene of the miR-451, was validated by fluorescent reporter assay. [score:2]
Using this assay, we demonstrated that CAB39 was a target gene of miR-451. [score:2]
miR-451 regulated PI3K/ATK pathway factors in human glioma in vitro. [score:2]
As shown in Fig. 4B, obvious activation of phosphorylated-AKT was observed in U251, LN229, A172 and U87 cells after transfection with the miR-451 mimics. [score:1]
Indeed, 22/22 low grade gliomas exhibited detectable levels of miR-451, while in 4/53 high grade gliomas miR-451 was at detectable levels (p<0.05) (Fig. 2C). [score:1]
When the tumors were approximately 5 mm in length, the mice were randomly divided into 3 groups (10 mice per group): the LN229 control group, the LN229 scramble PBS -treated group, and the LN229 miR-451 -treated group. [score:1]
hsa-miR-451 is located on chromosome 17q11.2, a region known to be amplified in certain types of cancers, in close proximity to ERBB2 (17q12) (16, 17). [score:1]
Tumors in the group treated with miR-451 maintained a slow growth rate throughout the experiment while tumors in the control group began to grow faster. [score:1]
The probes (miR-451 10 ng) were added to the sections on the microarray and incubated overnight at 40°C in a water bath. [score:1]
A mixture of 5 μl oligonucleotides containing scramble miR-451 mimics and 10 μl Lipofectamine was injected into the xenograft tumor mo del in a multi-site injection manner. [score:1]
The sequences of the LNA/DNA oligonucleotides contained locked nucleic acids at five consecutive centrally located bases (indicated by the underline) as shown: HSA-miR-451 5′- TTGAG TCATT ACCAT TGCCA AA-3′. [score:1]
Though the exact molecular mechanisms for glioma genesis remain unclear, recent studies have reported that there were several microRNA (miRNA or miR) abnormalities in human gliomas, including miR-451 (3). [score:1]
To further understand the anti-tumor effect of miR-451 and its role in the signaling pathway in vivo, we employed an LN229 xenograft glioma mouse mo del. [score:1]
The oligonucleotide sequence of the hsa-miR-451 mimics was: 5′-AAACCGUUACCAUUACUGAGUU-3′. [score:1]
miRNA-451 was one of them. [score:1]
Transfections with hsa-miR-451 mimics were performed in serum-free medium 24 h after plating, with Lipofectamine 2000 (Invitrogen). [score:1]
Finally, to further evaluate the possibility of AKT1 and c-Myc as hsa-miR-451 target genes we used RNAhybrid (http://bibiserv. [score:1]
During the first 3 days of observation following intratumoral administration of miR-451, tumors in both the control and treated groups grew slowly with no marked differences in tumor size between them. [score:1]
A tumor suppressive role of miR-451 was shown in gliomas in vitro (18), but whether or not miR-451 actually participated in gliomagenesis still needs further investigation. [score:1]
At the termination of the study, the difference in tumor mass between the miR-451 treated group and the control group was marked (p<0.01). [score:1]
[1 to 20 of 58 sentences]
2
[+] score: 158
miR-451 is downregulated in gastric cancer [26], breast cancer, and head and neck squamous cell carcinoma [27], where it executes tumor suppressor functions by targeting macrophage migration inhibitory factors and a disintegrin and metalloproteinase (ADAM) protein family members ADAMTS5 and ADAM10. [score:10]
Collectively, lincRNA-p21 overexpression by miR-451 MRE-regulated adenoviral vector suppresses the activation of β-catenin signaling in ALDH [+] CSCs in a miR-451 -dependent manner. [score:6]
These data suggest that integration of miR-451 MREs does not significantly suppress the expression of exogenous gene in CSCs while sparing normal cells. [score:5]
Four MREs of miR-451 were incorporated into lincRNA-p21 -expressing adenoviral vector (Ad-lnc-p21) to constrain its expression, which was designated as Ad-lnc-p21-MRE (Figure 3D). [score:5]
Luciferase activities were greatly suppressed by more than 92% in miR-451 -high -expressing NCM460 and L-02 cells that were transfected with psiCheck2-MRE (Figure 3C). [score:5]
These data imply that application of miR-451 MRE may prevent lincRNA-p21 expression in the normal tissues of the mice, thus reducing side-effects such as growth inhibition and apoptosis induction towards healthy cells. [score:5]
We demonstrated that MRE of tumor suppressor miRNAs could be exploited to enable specific transgene expression in CSCs and that miR-451 was such a candidate for CRC. [score:5]
miR-451 expression is dramatically reduced in ALDH [+] CSCsSeveral lines of evidence suggest that miR-451 acts as a tumor suppressor in multiple neoplasms [21, 25– 27]. [score:5]
Our results suggest that lincRNA-p21 is potentially applicable to eliminate CSCs and integration of miR-451 MREs significantly reduces its off-target expression in normal tissues. [score:5]
Incorporation of miR-451 MREs minimizes the off-target expression of lincRNA-p21 and its toxicities to normal hepatocytes. [score:5]
Specifically, inhibition of miR-451 facilitated efficient suppression of β-catenin signaling activity by Ad-lnc-p21-MRE in NCM460 cells (Figure 4B). [score:5]
Thus, we integrated MREs of miR-451 into the lincRNA-p21 -expressing adenovirus and low levels of miR-451 in CRC cells, especially ALDH [+] CSCs, allowed efficient introduction of lincRNA-p21, while high abundance of miR-451 avoided transgene expression in normal colon mucosal and liver cells in vitro and in vivo. [score:5]
Ad-lnc-p21-MRE suppresses β-catenin signaling in ALDH [+] CSCs in a miR-451 -dependent mannerLincRNA-p21 was shown to reduce the levels of β-catenin protein in HeLa cells [18], indicating lincRNA-p21 could also inhibit β-catenin signaling in CRC cells. [score:5]
B. NCM460 cells were transduced as in (A) The cells were co -transfected with the mixture of TOPFlash reporter plasmids and pRL-TK control plasmids (1 μg / 1 × 10 [6] cells; 40:1), and/or Wnt 3a -expressing plasmid (500 ng / 1 × 10 [6] cells) and miRNA-451 inhibitor (50 nM) for 48 hrs. [score:5]
A recent study showed that expression of miR-451 was significantly downregulated in CRC CSCs, as compared to the bulk tumor cells [21]. [score:5]
Ad-lnc-p21-MRE suppresses the activity of Wnt/β-catenin pathway in ALDH+ CSC in a miR-451-regulated manner. [score:4]
Collectively, we constructed a novel adenoviral vector that expressed lincRNA-p21 in a miR-451-regulated fashion. [score:4]
To address this issue, four copies of miR-451 MREs were inserted into the psiCheck2 plasmid for luciferase expression (psiCheck2-MRE). [score:3]
These data demonstrate that integration of miR-451 MREs enables specific and efficient expression of lincRNA-p21 in ALDH [+] CSCs. [score:3]
Ad-lnc-p21-MRE suppresses β-catenin signaling in ALDH [+] CSCs in a miR-451 -dependent manner. [score:3]
Application of miRNA response elements (MREs) of miR-451 prevents exogenous gene expression in normal cells. [score:3]
To detect miR-451 expression level, qPCR was performed using TaqMan® 2 × Universal PCR Master Mix (Applied Biosystems) on CFX96™ Real-Time PCR Detection System (Bio-Rad Laboratories, CA). [score:3]
In ALDH [−] non-CSCs, the application of miR-451 MREs caused only a moderate reduction in luciferase expression (21.4% in ALDH [−] HCT116 cells and 19.2% in ALDH [−] R KO cells) (Figure 3C). [score:3]
The remarkable differences in the abundance of miR-451 between ALDH [+] CSCs, ALDH [−] non-CSCs and normal cells make its MRE an attractive modulator to ensure the CRC-specific expression of exogenous therapeutic genes. [score:3]
Importantly, injection with Ad-lnc-p21-MRE did not elevate blood ALT levels in recipient mice (Figure 7I), suggesting that integration of miRNA-451 MRE in the adenovirus at least protected the naïve mice from hepatocyte damage induced by lincRNA-p21 overexpression. [score:3]
In addition, ALDH [+] CSCs exhibited much lower expression of miR-451 than ALDH [−] cells. [score:3]
miR-451 MRE -mediated delivery of lincRNA-p21 by adenovirus effectively suppresses malignant phenotypes of CRC CSCs in a cancer-specific fashion. [score:3]
Thus, we hypothesize that MREs of miR-451 may be utilized to specifically and efficiently deliver tumor suppressor lincRNAs into CSCs. [score:3]
miR-451 expression is dramatically reduced in ALDH [+] CSCs. [score:3]
Moreover, restoration of miR-451 expression rescued the activation of β-catenin signaling in ALDH [+] CRC cells infected with Ad-lnc-p21-MRE (Figure 4C). [score:3]
Several lines of evidence suggest that miR-451 acts as a tumor suppressor in multiple neoplasms [21, 25– 27]. [score:3]
The cells were co -transfected with the mixture of TOPFlash reporter plasmids and pRL-TK control plasmids (1 μg / 1 × 10 [6] cells; 40:1), with or without miRNA-451 inhibitor (50 nM). [score:3]
miR-451 MRE-regulated adenovirus specifically delivers lincRNA-p21 into CRC cells and CSCs. [score:2]
miR-451 MRE-regulated adenovirus exhibits CRC specificity and facilitates efficient delivery of lincRNA-p21 into CSCs. [score:2]
Furthermore, miR-451 negatively regulates self-renewal, tumorigenicity, and chemoresistance of colorectal CSCs [21]. [score:2]
Furthermore, reduced expressions of miR-451 in ADLH [+] CSCs were observed even after serial passages in vitro, as compared to the corresponding ALDH [−] cells (Supplementary Figure S3A). [score:2]
We also observed that miR-451 expression levels were significantly reduced in CRC tissues compared with normal colorectal epithelia, and inversely correlated with the grades of CRC tumors (Figure 3A). [score:2]
TOPFlash reporter assays confirmed the suppression of Wnt/β-catenin signaling by Ad-lnc-p21-MRE, which could be as efficient as Ad-lnc-p21, and was tightly controlled by endogenous miR-451 in cells. [score:2]
Moreover, expression levels of miR-451 were decreased in all examined colorectal cancer cells, as compared to NCM460 normal colon mucosal cells and L-02 normal hepatocytes (P < 0.01) (Figure 3B). [score:2]
B. The levels of miR-451 were quantified by qPCR in normal cell lines and ALDH [+] or ALDH [−] subsets of CRC cells. [score:1]
D. Four copies of miR-451 MREs were inserted immediately following a lincRNA-p21-coding ORF on adenoviral vector Ad-lnc-p21 to generate Ad-nc-p21-MRE. [score:1]
A recombinant adenoviral vector armed with MREs of miR-451 immediately following the lincRNA-p21-coding open reading frame (ORF) (Ad-lnc-p21-MRE) was constructed. [score:1]
Here, we observed that miR-451 levels were significantly reduced in CRC cells. [score:1]
Additionally, the levels of miR-451 are reduced in cancer cells to facilitate both chemo- and radio- resistance [25, 36]. [score:1]
C. Luciferase activity was detected in indicated types of cells after transfection with psiCheck (1 μg / 1 × 10 [6] cells) and psiCheck2-miR-451-MRE (1 μg / 1 × 10 [6] cells) for 48 hrs. [score:1]
Figure 3 A. The expression levels of miR-451 in normal mucosa and CRC samples of distinct grades of differentiation (Inter, intermediate; undif, undifferentiated) were measured by qPCR. [score:1]
A. The expression levels of miR-451 in normal mucosa and CRC samples of distinct grades of differentiation (Inter, intermediate; undif, undifferentiated) were measured by qPCR. [score:1]
To generate Ad-lnc-p21-MRE, the DNA fragment containing 4 copies of MREs of miR-451 was inserted into pShuttle-CMV-lincRNA-p21 to generate pShuttle-CMV-lincRNA-p21-MRE and then package Ad-lnc-p21-MRE. [score:1]
Importantly, ALDH [+] CSCs contained even lower levels of miR-451 than ALDH [−] non-CSCs (Figure 3B). [score:1]
[1 to 20 of 49 sentences]
3
[+] score: 145
We further demonstrate that these dietary miR-451 molecules existing in the blood stream, even at very low levels, are capable of inhibiting their target gene expression in animals. [score:7]
Thus, miR-451 even at a very low concentration inhibits 14-3-3ζ protein expression by interacting directly with its 3′UTR of mRNA. [score:6]
To investigate further whether trace amount of miR-451 is sufficient to inhibit gene expression, the 3′UTR of Ywhaz/14-3-3ζ mRNA was linked to the protein-coding region of luciferase cDNA, and the luciferase reporter was transfected along with different amounts of miR-451 expression construct into S17, a stromal cell line derived from mouse bone marrow [28]. [score:5]
It is particularly true for miRNAs including miR-451 whose levels could be very low in KO animals but could still have a profound inhibitory effect on their target genes. [score:5]
The protein level of 14-3-3ζ, previously confirmed as a direct target of miR-451 by our laboratory [20], and two downstream anti-oxidant enzymes (Cat and Gpx1) were examined. [score:4]
We also use a luciferase report assay to show that a limited amount of miR-451 is enough to inhibit gene expression. [score:4]
In addition, gavage-feeding miR-144/451 mutant mice with WT blood cells that express abundant miR-144/451 elevates both miR-451 and miR-144 levels in miR-144/451 KO blood. [score:3]
The expression levels of miR-451 48 hours after transfection were confirmed using qRT-PCR (Supplementary Figure 4A). [score:3]
Furthermore, the increased mature miR-451 molecules in miR-144/451 KO blood enhance the anti-oxidant ability of erythroid cells by suppressing 14-3-3ζ and thus allowing the transcription of two anti-oxidant genes— cat and gpx1. [score:3]
Quantitative PCR analysis of miR-451 expression after gavage-feeding cooked chicken blood (B) fresh chicken blood (C) cooked pig blood (D) and fresh pig blood (E). [score:3]
Dietary miR-451 protects against oxidant stress in miR-144/451 KO erythroid cellsAs our laboratory and others have previously demonstrated, the protective role of miR-451 in erythropoiesis is due, at least partially, to its ability to mediate the inhibition of the cytoplasmic adaptor protein 14-3-3ζ [20, 27]. [score:3]
Fusion of the Ywhaz/14-3-3ζ 3′UTR to luciferase cDNA, along with as low as 0.025 ng/ml of miR-451 retroviral vector, dramatically decreased enzymatic activity in transfected S17 cells, presumably reflecting decreased luciferase protein expression (Supplementary Figure 4B). [score:3]
miR-451 at the concentration of 0.25 ng/ml reached the maximum inhibition of luciferase activity (Supplementary Figure 4B). [score:3]
As our laboratory and others have previously demonstrated, the protective role of miR-451 in erythropoiesis is due, at least partially, to its ability to mediate the inhibition of the cytoplasmic adaptor protein 14-3-3ζ [20, 27]. [score:3]
Another interesting finding in our study is that although miR-144/451 genes have been knocked out, blood in miR-144/451 KO mice fed with regular chow diet still contains low levels of miR-451. [score:2]
These results clearly indicate that ingestion of at least some miRNAs, such as miR-451, affects the function of the consumers, suggesting that regulatory information, whether detrimental to or beneficial for health, could be inherited from ingested reagents including everyday food products, nutrient supplements and small RNA interfering drugs. [score:2]
To make miR-451 expression vector, genomic fragments encompassing mouse miR-451 (272 bp) were cloned into MSCV-PIG retroviral vector by PCR using the primers engineered with XhoI and EcoRI restriction sites (sequences listed in Supplementary Table 1). [score:2]
Figure 7Exogenous miR-451 existing in miR-144/451 KO mice enhances anti-oxidant activity in vivo via increasing the activity of Foxo3 pathway (A) Bone marrow erythroblasts were fractionated according to the developmental markers Ter119, CD71, and forward scatter (FSC) intensity. [score:2]
Here we use a simple animal mo del, miR-144/451 gene knockout (KO) mice [20], to clearly demonstrate that ingestion of wild type (WT) blood, that contains abundant miR-451 and miR-144, significantly increases the level of miR-451 and miR-144 in the circulation of miR-144/451 mutant mice. [score:2]
This data clearly indicates that the extra level of miR-451 derived from food intake regulates the 14-3-3ζ/Foxo3 signaling pathway. [score:2]
In current study, we found that the mouse digestive system allows different degrees of miRNA uptake (miR-451 vs. [score:1]
Co-transfection of Renilla vectors and Ywhaz/14-3-3ζ 3’-UTR luciferase reporter plasmid to S17 mouse bone marrow stromal cells with or without the miR-451 retroviral vector was performed using Lipofectamine 2000 (Invitrogen Life Technologies). [score:1]
Both qRT-PCR methods, using small nuclear RNA U6 (snRU6, or U6) as internal loading control, showed that the miR-451 level in peripheral blood of miR-144/451 KO mice rapidly climbed after feeding WT blood and reached a peak after 6 hours (Figure 1A-1C). [score:1]
These results confirm that miR-144/451 KO mice still contain miR-451 primarily coming from the mouse chow diet. [score:1]
These diet-derived miR-451 are stable for at least three weeks when the chow diet is kept at room temperature (data not shown). [score:1]
The acid treatment failed to significantly change the yield of miR-451 from WT mouse blood (Supplementary Figure 3A-3B). [score:1]
As expected, the sequence for mature miR-451 (blue color) followed by a poly-A sequence (a link sequence for reverse transcription, red color) existed in PCR products (Figure 1E), confirming that the mature miR-451 molecules were in the circulation of miR-144/451 KO mice. [score:1]
Consistent to the results from administration of WT mouse blood, the level of miR-451 was significantly elevated after ingestion of chicken or pig blood (Figure 2B-2E). [score:1]
To mimic food processing, an experiment was set to determine whether heating or regular cooking (95°C for 10 min) could degrade miR-451. [score:1]
Without the diet-derived miR-451, mutant red blood cells are more susceptible to oxidant stress -induced injury. [score:1]
Ingestion of wild type blood from chickens and pigs increases the level of miR-451 in peripheral blood of miR-144/451 KO mice. [score:1]
These results clearly indicate that exogenous miR-451 can enter the circulation through the mouse digestive system. [score:1]
The level of miR-451 decreased three-fold in the first week and four-fold after two weeks (Figure 5C), indicating that the miR-451 was reduced to levels that make detection difficult. [score:1]
Figure 4RNase degrades miR-451 efficiently in vitroTotal RNA from WT blood was treated with RNase A at different concentrations for 30 min at room temperature. [score:1]
As shown in Supplementary Figure 2, there was no significant difference of miR-451 levels between fresh and cooked blood from three different species (mouse, chicken and pig). [score:1]
Since mice can uptake miR-451 from a regular chow diet, which contains miR-451 (Figure 5A-5B), we decided to feed mice with a special diet that replaced the fish powder with corn and soybean supplements for 20 and 40 days. [score:1]
Given that miR-451 is highly conserved among different species such as human, mouse and many different types of fishes including zebra fish, we hypothesized that miR-144/451 KO mice might uptake food-derived miR-451. [score:1]
Interestingly, there are only several folds more miR-451 in WT urine than miR-144/451 KO urine (Figure 5D–5E), suggesting that miR-144/451 undergo catabolism before clearance by urinary system. [score:1]
To examine whether miR-451 from chickens and pigs, two animals most common in human diets, can go through the mouse digestive system, blood from chicken and pig, either fresh or cooked, were gavage fed to miR-144/451 KO mice. [score:1]
Synthetic miR-451 oligonucleotides were purchased from Takara Bio. [score:1]
Since the average threshold cycle (C [T]) per PCR reaction for miR-144/451 KO blood sample was around 30, we estimated that the copy number of miR-451 in miR-144/451 KO blood before and after gavage feeding of WT blood were 1.07 x 10 [5] copies/μl and 4.28 x 10 [6] copies/μl blood, respectively. [score:1]
Dietary miR-451 protects against oxidant stress in miR-144/451 KO erythroid cells. [score:1]
miR-451 level in miR-144/451 KO blood was used as control and assigned a relative value of 1. (C) qRT-PCR analysis of blood miR-451 level in miR-144/451 KO mice after feeding with a special chow diet that contains a very low level of miR-451 (B). [score:1]
To examine whether the PCR signals are from miR-451, PCR products from miR-144/451 KO blood, either before or after gavage feeding of WT blood, were gel-purified, engineered to TA cloning vector and sequenced. [score:1]
miR-451 levels in the urine of miR-144/451 KO mice are similar to the ones in miR-144/451 KO blood (C [T] value around 30). [score:1]
However, miR-451 can be easily degraded by RNase though the stability is higher than that of U6 control RNA. [score:1]
In this study we utilize this mouse mo del to show that oral ingestion of WT blood leads to increased miR-451 and miR-144 levels in the circulating blood of miR-144/451 KO mice. [score:1]
The level of miR-451 in serum depleted of exosomes with ultracentrifugation (120,000g for 2 hours) was in undetectable range (data not shown). [score:1]
As expected, RNase treatment significantly affected the stability of miR-451 in a dose dependent manner and even trace amount of RNase (15.6 ng/ml) degraded miR-451 by an order of magnitude (Figure 4A). [score:1]
Analysis of C [T] value (D) and relative level (E) of miR-451 in mouse urine. [score:1]
Our data clearly indicates that miR-451 in food can pass through the digestive system to enter the bloodstream and protect the red blood cells. [score:1]
The Y-axis shows the C [T] value of miR-451. [score:1]
This data suggests that exosomes may be the transportation vesicle for miR-144/451 transferring from the GI tract into peripheral blood, or at least, exosomes are used as the transportation vesicles by miR-451 molecules when they are circulating in vascular system. [score:1]
Figure 2Ingestion of wild type blood from chickens and pigs increases the level of miR-451 in peripheral blood of miR-144/451 KO mice (A) Multispecies nucleotide sequence alignments showing complete conservation of mature miR-451 in mouse, chicken and pig. [score:1]
Moreover, alteration of erythroid phenotypes can be accomplished by either lowering (special chow diet) or by increasing (gavage-feeding WT blood) the miR-451 level in miR-144/451 KO blood. [score:1]
To examine whether the potentially existent miR-451 in miR-144/451 KO blood was from food uptake, the miR-144/451 KO mice originally fed with a regular chow diet were fed with the special chow diet. [score:1]
Ingestion of wild type blood increases the levels of miR-451 and miR-144 in peripheral blood of miR-144/451 null mice. [score:1]
Figure 5Chow diet-derived miR-451 is present in miR-144/451 KO miceAnalysis of (A) C [T] value and (B) relative level of miR-451 in different mouse chow diet. [score:1]
This miRNA mainly comes from the regular mouse chow diet that contains animal-derived, presumably fish-derived miR-451. [score:1]
Note: miR-451 survives degradation by RNase better than U6. [score:1]
Our previous study shows that miR-451 and miR-144 are encoded by a bicistronic miRNA locus transcriptionally controlled by GATA1, a “master” nuclear factor in erythroid cells [21]. [score:1]
This data suggest that miR-451, even at a very low level, can significantly reduce hemolysis of miR-144/451 KO erythroid cells. [score:1]
This explains, at least in part, that oral administration of WT blood allows only limited access of miR-451 and miR-144 to the circulation of miR-144/451 KO animals. [score:1]
Specifically, miR-451 comprises about 50% of the total miRNA pool in murine erythrocytes as reported by an RNA sequencing study [22]. [score:1]
The Y-axis shows the C [T] value of miR-451 (G) and fold change of miR-451 with the miR-451 level at zero hour (KO) assigned as a relative value of 1 (H). [score:1]
Note: the sequence highlighted with blue color is the sequence of mature miR-451 and the poly A highlighted with red color is the adapter sequence for reverse transcription. [score:1]
Figure 6Change of anemic phenotypes of miR-144/451 KO mice after feeding with wild type blood or special chow diet containing much less miR-451 (A) Hydrogen peroxide (H2O2) -induced color change of miR-144/451 KO blood with and without feeding with WT blood. [score:1]
No significant difference of miR-451 levels between alkaline solution treated and untreated RNA was observed (Supplementary Figure 3C-3D). [score:1]
For example, copy number of miR-451 per μl of miR-144/451 KO blood at 30 C [T] = [21415 copies x (100 μl total RT products / 2 μl RT products used for PCR) x (50 μl total RNA from 200 μl blood / 2.5 μl RNA used for RT)]/200 μl blood = 107035 copies/μl. [score:1]
X-axis shows the concentrations of RNase A. As expected, RNase treatment significantly affects the stability of miR-451 in a dose dependent manner. [score:1]
The Y-axis shows relative fold change of miR-451 with the miR-451 level at zero hour assigned as a relative value of 1. X-axis shows hours after feeding WT blood. [score:1]
Figure 1Ingestion of wild type blood increases the levels of miR-451 and miR-144 in peripheral blood of miR-144/451 null mice (A) Schematic view for the ingestion of WT blood into miR-144/451 KO mice. [score:1]
Consistent to these findings, our experiments have confirmed that miR-451 is extremely stable under highly acidic, alkaline and hot conditions. [score:1]
The Y-axis shows relative levels of miR-451 in miR-144/451 KO blood. [score:1]
Ribonuclease degrades miR-451 efficiently in vitro. [score:1]
miR-451 level in miR-144/451 KO blood was used as control. [score:1]
Ingestion of wild type blood increases the levels of miR-451 and miR-144 in peripheral blood of miR-144/451 null miceOur previous study shows that miR-451 and miR-144 are encoded by a bicistronic miRNA locus transcriptionally controlled by GATA1, a “master” nuclear factor in erythroid cells [21]. [score:1]
RNase degrades miR-451 efficiently in vitro. [score:1]
miR-144/451 KO mice lacking of a 388 bp segment of genomic DNA containing the bicistronic miR-144 and miR-451 locus was described in our published work [20]. [score:1]
Exogenous miR-451 existing in miR-144/451 KO mice enhances anti-oxidant activity in vivo via increasing the activity of Foxo3 pathway. [score:1]
In addition, miR-451 can be sufficiently detected in the circulating blood of miR-144/451 KO mice fed with regular mouse chow diet. [score:1]
The data indicates that miR-451 can survive high temperature, acidification, and alkaline conditions. [score:1]
Whereas feeding miR-144/451 KO mice with a chow diet containing less miR-451 reduces the miR-451 level in miR-144/451 KO blood. [score:1]
After feeding with WT blood, the C [T] was down about 6 cycles, meaning miR-451 increased 60 fold (Figure 1G–1H). [score:1]
and diluted in water as stocking solution at the concentration of 32 pg/ml, with estimated 2.74112x10 [9] miR-451 copies/ml. [score:1]
To estimate the copy numbers of mature miR-451 that existed in miR-144/451 KO blood, a standard curve was made using synthetic miR-451 as input ranging from 0.015625 pg/μl (equivalent to 1338 copies) to 4 pg/μl (equivalent to 685280 copies, http://www. [score:1]
Change of anemic phenotypes of miR-144/451 KO mice after feeding with wild type blood or special chow diet containing much less miR-451. [score:1]
Reducing miR-451 level in miR-144/451 KO blood, by feeding a special food that contains much less miR-451, accelerates microcytosis. [score:1]
The Y-axis shows relative level of miR-451 in miR-144/451 KO blood. [score:1]
The degree of the miR-451 increase in miR-144/451 KO blood was dependent on the amount of blood orally received by the miR-144/451 KO mice, and administrating 200-400 μl of blood gave the maximum increase of miR-451 in blood (Figure 1D). [score:1]
To examine whether RNase destroys miR-451, total RNA from fresh WT blood was treated with different concentrations of RNase for 30 min. [score:1]
RNase at the concentration of 31.3 ng/ml degraded U6 about 26 times more than miR-451 (Figure 4B). [score:1]
Chow diet-derived miR-451 is present in miR-144/451 KO mice. [score:1]
Interestingly, feeding synthetic miR-451 to miR-144/451 KO mice also increased the miR-451 level in miR-144/451 KO blood, but the degree of which miR-451 increased was far less than when fed with WT blood (Supplementary Figure 1A-1B). [score:1]
The sequences of mature miR-451 are 100% identical among mice, chickens and pigs (Figure 2A). [score:1]
Analysis of (A) C [T] value and (B) relative level of miR-451 in different mouse chow diet. [score:1]
Although the protection was far less than that of the WT control (light blue line in Figure 6B), it still indicates that the elevated miR-451 level in miR-144/451 KO mice helps to protect erythrocytes from oxidant stress induced hemolysis. [score:1]
In conclusion, we use a very simple and an easily reproduced animal mo del, the miR-144/451 KO mo del, to show that miR-451 is sufficiently detected in the circulating blood of miR-144/451 KO mice fed with regular chow diet that contains well conserved miR-451. [score:1]
[1 to 20 of 98 sentences]
4
[+] score: 139
Expression of miRNAs in whole blood, serum and WBCs following LTA injection was quantified using real-time RT-PCR to verify selected up-regulated miRNA targets with at least 2-fold increase in expression (miR-451, miR-668, miR-1902, and miR-1904). [score:10]
The results showed that LPS significantly induced miR-451 expression at concentrations of 10, 100 and 1000 μg but not up-regulated the expression of the other 3 miRNA targets (Figure 5). [score:10]
Previously, we had identified a specific whole blood–derived miRNA signature in mice exposed to LPS as there was a dose- and time -dependent upregulated expression of the miRNA targets (let-7d, miR-15b, miR-16, miR-25, miR-92a, miR-103, miR-107 and miR-451) follo-wing in vivo LPS injection [14]. [score:8]
Besides, LTA did not up-regulate the expression of these miRNA targets, except miR-451, in the concentration up to 1000 ug [14]. [score:8]
First, LPS is a stronger stimulator than LTA to induce the expression of circulating miRNAs, considering the up-regulated 8 miRNAs of the whole blood showed approximately 5- to 12-fold increase in expression 6 h after 100 and 1000 μg LPS injection, these four miRNAs (miR-451, miR-668, miR-1902, and miR-1904) had a less prominent 2- to 6-fold increase upon LTA treatment. [score:8]
The up-regulated miRNA targets more than double of those of the control is shown in Table 1. There were 4 miRNAs (miR-451, miR-668, miR-1902, and miR-1904) showed significantly increased expression in the whole blood of mice exposed to LTA originated from different Gram -positive bacteria. [score:8]
In contrast to the expression of miR-451, miR-1902, miR-1904, but not miR-668, in serum of C57BL/6 at 6 h after exposure to 100 μg of LTA, no significantly up-regulation of these 4 miRNA targets was detected in the WBCs after LTA injection, when compared with those in C57BL/6 receiving PBS injection (Figure 4A). [score:7]
Additionally, LPS significantly induced miR-451 expression at concentrations of 10, 100 and 1000 μg but not increase the expression of the other 3 miRNA targets. [score:7]
Using real-time RT-PCR, the expression of the up-regulated miR-451, miR-668, miR-1902 and miR-1904 identified using miRNA microarray was detected in the whole blood at 6 h following injection of 10, 100, 1000 μg of LTA; mice were killed at the indicated survival times (2, 6, 24, and 72 h) following 100 μg of LTA injection. [score:6]
Using real-time RT-PCR, the expression of the up-regulated miR-451, miR-668, miR-1902 and miR-1904 was detected in the serum at 6 h following injection of 10, 100, 1000 μg of LTA; mice were killed at the indicated survival times (2, 6, 24, and 72 h) following 100 μg of LTA injection. [score:6]
In Tlr2 [−/−] mice, significantly higher expression of miR-451, miR-668, miR-1902, and miR-1904 in the serum were observed following LTA injection with around 6- to 10-fold of expression against that from the Tlr2 [−/−] mice injected with PBS (Figure 4B). [score:5]
In contrast, LPS exposure induced moderate expression of miR-451 but not of the other 3 miRNA targets. [score:5]
In contrast, LTA exposure induced moderate expression of miR-451 but not of the other 7 miRNA targets [14]. [score:5]
In addition, at 24 h, only miR-1902, but not miR-451 which was observed in the whole blood, continued to be significantly expressed in the serum (Figure 3B). [score:3]
However, in this study, higher expression of miR-451, miR-668, miR-1902, and miR-1904 in the serum were observed in Tlr2 [−/−] against C57BL/6 mice following LTA injection. [score:3]
miR-451 had also been found to direct a negative regulatory cascade to tune the cytokine production of dendritic cells including IL-6, TNF, CCL5/RANTES, and CCL3/MIP1α [16]. [score:3]
In the whole blood, following injection with 10 μg of LTA, there was significantly increased expression in miR-1902, but not in miR-451, miR-668 or miR-1904 (Figure 2A). [score:3]
Upon 100 ug of LTA injection, significantly increased expression around 2- to 3-fold was observed in miR-451, miR-1902, and miR-1904, but not in miR-668 (Figure 2A). [score:3]
Among these 4 miRNA targets, miR-451 had been reported to be a promising biomarker for microRNAs involved in lung tissue infected with pathogen as Actinobacillus pleuropneumoniae[15]. [score:3]
Whether the higher expression of miR-451, miR-668, miR-1902, and miR-1904 in the serum upon LTA stimulation is due to lack of the repressed targets of negative feedback loop in Tlr2 [−/−] mice is speculated but lack of evidence so far and required further investigation and validation. [score:3]
At 24 h, only miR-451 continued to be significantly expressed in the whole blood (Figure 2B). [score:3]
In previous study, we had demonstrated that expression of multiple miRNAs (let-7d, miR-15b, miR-16, miR-25, miR-92a, miR-103, miR-107, and miR-451) is significantly altered in the whole blood of mice after exposure to LPS in a dose- and time -dependent fashion [14]. [score:3]
When exposed to 1000 ug of LTA, all these four miRNAs (miR-451, miR-668, miR-1902, and miR-1904) had a significant expression around 3- to 6-fold than the control (Figure 2A). [score:3]
Notably, miR-451 was both induced by LPS and LTA treatment in this study and the expression of miR-668 was significantly induced in the whole blood and in the serum by the high dose of LTA in 1000 ug concentration, but not by lower to medium dose of LTA in 10 and 100 ug concentrations. [score:3]
In this study, we demonstrated that expression of miR-451, miR-668, miR-1902, and miR-1904 is significantly altered in the whole blood and serum of mice after exposure to LTA in a dose- and time -dependent fashion. [score:3]
Figure 4 Expression of miR-451, miR-668, miR-1902, and miR-1904 of serum and WBCs from C57BL/6 and Tlr2 [−/− ] mice from real-time RT-PCR experiments 6 h after exposure to 100 μg of LTA or phosphate-buffered saline (PBS); **, P < 0.01 vs. [score:3]
Figure 5 Expression of miR-451, miR-668, miR-1902, and miR-1904 of serum from C57BL/6 mice using real-time RT-PCR experiments 6 h after exposure to 10, 100, and 1000 μg LPS from Escherichia coli serotype 026:B6; *, P < 0.05 vs. [score:3]
A significant increase of 4 miRNAs (miR-451, miR-668, miR-1902, and miR-1904) was observed in the whole blood and the serum in a dose- and time -dependent fashion following LTA injection. [score:1]
Induction of miR-451, miR-1902, and miR-19042, but not miR-668, was evident at 6 h following injection with 100 ug of LTA (Figure 2B). [score:1]
To investigate that whether LPS originating from Gram -negative bacteria Escherichia coli serotype 026:B6 (L3755) induces expression of miR-451, miR-668, miR-1902, and miR-1904, the serum was obtained for real-time PCR at 6 h following intraperitoneal injections of 10, 100, or 1000 μg LPS. [score:1]
Therefore, the use of miR-451 or miR-668 as a biomarker to differentiate the exposure to LPS or LTA is not suitable. [score:1]
[1 to 20 of 31 sentences]
5
[+] score: 110
The downregulation of miR451 target proteins, induced by MV-HLSC, was abrogated when HepG2 were transfected with anti-451 miRNA inhibitor. [score:8]
When HepG2 were transfected with the miRNA inhibitor, anti-miR451, MVs were unable to downregulate the MDR1 expression, suggesting that miR451 transferred by MVs was biologically active. [score:8]
The most convincing results were obtained with inhibitors of miR31 and 223 that were downregulated also in MV DCR− as well as with the inhibitor of miR451, that has been previously described as a Dicer independent miRNA [56]. [score:8]
Supporting Information Figure 3B shows that MDR1, MIF, and RAB14, targeted by miR451, and E2F-2, targeted by miR31, were overexpressed at RNA level in HepG2 with respect to hepatocytes. [score:7]
We also observed that the HepG2 stimulation with MV-HLSC induced a downregulation of two other important miR451 targets, MIF and RAB14 (Fig. 5D) [40, 41]. [score:6]
Transfection of HepG2 with anti-miR451 (anti-miR451+MV) but not with anti-CTR abrogated the target downregulation induced by MV-HLSC. [score:6]
HepG2 stimulation with MV-HLSC induced a downregulation of MIF and RAB14, previously shown to be important miR451 targets [39, 40]. [score:6]
As shown in Figure 5D, MDR1, targeted by miR451 [40], was strongly expressed on HepG2 cell membrane. [score:5]
The prominent role of miR451 and miR31 transfer was indicated by the direct antitumor activity of miR451 and miR31 mimics on HepG2 that resulted in MDR1, MIF, RAB14, and E2F-2 downregulation similar to that of MV-HLSC. [score:5]
Treatment with anti-miR451 and anti-miR31 in the absence of MVs did not interfere with target expression by hepatoma tumors. [score:5]
In particular, we analyzed the involvement in MV-HLSC antitumor activity of miR31 and miR451, previously described as regulators of proliferation and as tumor suppressors in different cancer cells [35, 38, 39]. [score:4]
Their downregulation, induced by MVs, was abrogated when HepG2 were transfected with anti-miR451, but not with anti-CTR (Fig. 5D). [score:4]
Furthermore, HepG2 transfection with miR451 and miR31 mimics resulted in MDR1, MIF, RAB14, and E2F-2 downregulation similar to that of MV-HLSC (Fig. 5D, 5E). [score:4]
In mice treated with anti-miR451 and anti-miR31, the inhibition of tumor growth induced by MV-HLSC was significantly less effective than in animals treated with anti-CTR (Fig. 6, A– 6C). [score:3]
MVs from fibroblasts, used as control, contained significant less amount of tumor suppressive miR451, 223, and 31, than MV-HLSC (Fig. 3C). [score:3]
In Vivo Biological Effect of Anti-miR451 or Anti-miR31 Inhibitors. [score:3]
Transfection of HepG2 with anti-miR451 without MV treatment, did not affect MDR1 expression (data not shown). [score:3]
Moreover, the use of miRNA inhibitors against miR451, miR223, miR24, miR125b, and miR31 on HepG2 reduced the proapoptotic activity induced by MV-HLSC. [score:3]
As shown in Figure 3C, the content of tumor-suppressive miRNAs miR451, 223, and 31, in MVs from fibroblast used as control was significantly lower than that of MV-HLSC. [score:3]
The inhibitory effect of MV-HLSC was abrogated by anti-miR451 and anti-miR31 administration (Fig. 6E, 6F). [score:3]
Treatment with anti-miR451 without MV administration (anti-miR451) did not interfere with protein expression by HepG2. [score:3]
HepG2 transfection with miR451, miR31, and miR223 mimics, which reproduce mature endogenous miRNAs, inhibited proliferation of HepG2 (Fig. 5B). [score:3]
Moreover, the miR451 has been shown to regulate drug resistance to chemotherapeutics mediated by MDR1/P-glycoprotein [41]. [score:2]
Among miRNAs present in MV-HLSC, we detected several miRNAs with potential antitumor activity including miR451, miR223, miR24, miR125b miR31, and miR122 (Fig. 3A). [score:1]
The miR451 mimic mediated also a proapoptotic effect comparable to that of MV-HLSC (Fig. 5C). [score:1]
Among miRNAs present in MV-HLSC [10], several ones were associated with potential antitumor activity, such as miR451, miR223, miR24, miR125b, miR31, miR214, and miR122. [score:1]
This was more significant for miR451, miR223, and miR31. [score:1]
To evaluate whether single miRNAs with antitumor activity (miR451, miR223, miR24, miR125b, and miR31) were relevant for the proapoptotic effect of MV-HLSC, we transfected HepG2 with selected miRNA inhibitors (Fig. 5A). [score:1]
[1 to 20 of 28 sentences]
6
[+] score: 80
Expression of miR-451 in P. berghei-infected mouse erythrocytesIn addition to Homo sapiens, miR-451 is also expressed in other species, such as Mus musculus, Rattus norvegicus, Danio rerio, Xenopus tropicalis, Gallus gallus, and Mono delphis domestica [26]. [score:5]
The association between miR-451 expression level and the development of erythrocyte-stage P. falciparum. [score:4]
In this study, the expression of miR-451 in the blood of KM mice was confirmed by (Figure 3). [score:3]
Further analysis of miR-451 expression and malaria infection showed no association between the accumulation of miR-451 in Plasmodium falciparum-iRBCs, the life cycle stage of P. falciparum in the erythrocyte, or of P. berghei in mice. [score:3]
However, a human miRNA, miR-451, was highly expressed, comprising approximately one third of the total identified miRNAs. [score:3]
QZ carried out Northern blot of miR-451 expression. [score:3]
siRNAs: short interfering RNAs; RISC: RNA -induced silencing complex; iRBCs: infected red blood cells; ASO: antisense oligonucleotide; WBC: white blood cells; has: Homo sapiens;LNA: locked nucleic acids XX carried out the construction and analysis of small RNA library, participated in the analysis of miR-451 expression and drafted the manuscript. [score:3]
The weaker expression of miR-451 in higher parasitaemia, as detected by Northern blotting, is due to dilution of parasite RNAs, because this difference was abolished after adjusting the total RNAs loaded based on the number of blood cells. [score:3]
In addition, an ASO against miR-451, which normally inhibits miRNA activity [28- 30], had no observable effects on the growth of P. falciparum. [score:3]
The association between miR-451 expression and the parasite were analysed by Northern blotting and antisense oligonucleotide (ASO) of miR-451. [score:3]
Figure 2 Detection of expression of miR-451 by Northern blot. [score:3]
In addition to Homo sapiens, miR-451 is also expressed in other species, such as Mus musculus, Rattus norvegicus, Danio rerio, Xenopus tropicalis, Gallus gallus, and Mono delphis domestica [26]. [score:3]
The results showed that miR-451 expression, when comparing equivalent amounts of RNA, decreased slightly from lower to higher parasitaemia and became undetectable at 86% parasitaemia (Figure 3A). [score:3]
Figure 3Analysis of miR-451 expression in the blood of P. berghei-infected KM mice at different parasitaemias. [score:3]
Several potential explanations need to be addressed in future studies: (1) the ASO failed to diffuse into the RBCs, presumably due to their integration in the cell membrane of RBCs and the presence of nuclease in medium; (2) the accumulation of miR-451 to a very high level in RBCs abolished the inhibitory function of the ASO, even the ASOs that could enter the cells; (3) the lower affinity of the locked nucleic acid (LNA/DNA) miR-451 ASO might influence the formation of stable complexes with the blocking oligonucleotide [31]. [score:3]
When the parasitaemia in the mice reached approximately 10%, the blood was harvested for detecting expression of miR-451. [score:3]
The data presented here showed that accumulation of miR-451 in RBCs is unrelated to the life cycle of P. falciparum in the erythrocytic stage and parasitaemia in vivo, which suggested that the miR-451 expressed at high levels in RBCs is independent of parasite infection. [score:3]
So the relationship between malaria infection and the expression of miR-451 were further explored. [score:3]
Expression of miR-451 in P. berghei-infected mouse erythrocytes. [score:3]
To investigate the association between the expression level of miR-451 and parasite development, the transcription of miR-451 at different development stages of synchronized P. falciparum-infected RBCs was assayed by Northern blot. [score:2]
To further analyse the potential functions of miR-451 in the development of erythrocyte-stage parasites, the Plasmodium-infected RBCs were synchronized and cultured in RPMI-1640 medium containing an ASO of miR-451 (Sangon, Shanghai, China)[22]. [score:2]
The anti-miR-451 LNA oligonucleotide 5'-aaActCagTaaTggTaaCggTtt-3' (uppercase: LNA; lowercase: DNA) was complementary to the mature miR-451 sequence. [score:1]
Biotin-labeled miR-451 was used as a hybridization probe. [score:1]
Synthesis and administration of miR-451 antisense oligos (ASO). [score:1]
The investigation whether the expression of miR-451 could be influenced by Plasmodium infection in vivo was performed by using the P. berghei (ANKA strain) mice mo del. [score:1]
The human miR-451 accumulated at a very high level, comprising almost 1/3 of the identified miRNAs isolated from P. falciparum-iRBCs (Table 1). [score:1]
This indicated that the weak signal of the miR-451 transcript in samples with higher parasitaemia was due to dilution of parasite RNAs. [score:1]
After incubating with different concentrations of the miR-451 ASO for 72 hr, thin blood smears were prepared to determine parasitaemia of each sample by counting the number of parasites in 2,000 erythrocytes. [score:1]
Moreover, when total RNA from equivalent numbers of erythrocytes was loaded, there was also no significant difference among them, although the transcription level of miR-451 seemed slightly lower in the next generation (cultivated after 72 h) (Figure 2B). [score:1]
Moreover, treatment with an antisense oligonucleotide to miR-451 had no significant effect on the growth of the erythrocytic-stage P. falciparum. [score:1]
In addition, the miR-451 accumulation in Plasmodium-infected RBCs is independent of parasite infection. [score:1]
confirmed the abundance of miR-451 in Plasmodium-infected RBCs. [score:1]
Different concentrations of the miR-451 ASO were added to the cultures and parasitaemias were determined. [score:1]
The result showed that miR-451 was transcribed at a very high level in P. falciparum-iRBCs, whereas no miR-451 transcripts were observed in human WBCs (Figure 2A). [score:1]
However, if the total RNAs loaded were adjusted based on the number of blood cells, the difference in miR-451 transcript level disappeared (Figure 3B). [score:1]
To eliminate the possibility that the accumulated miR-451 in P. falciparum-iRBCs were derived from contamination by human white blood cells (WBCs), the transcription of miR-451 in parasite-iRBC and human WBCs was analysed by Northern blot. [score:1]
Notably, the miRNA miR-451 accumulated to a very high level in infected RBCs, comprising more than one third of the cloned miRNAs. [score:1]
[1 to 20 of 37 sentences]
7
[+] score: 78
S5 Fig(A) Microarray transcriptional analysis of LET1 cells stably expressing miR-144, miR-451, or vector alone were infected with influenza virus for 1 h. The heatmap depicts fold-change relative to a vector control for the set of genes whose expression in TC-1 cells following influenza virus infection was affected more than 2-fold (p<0.05) by miR-144/451 over -expression (Fig 3A) with red and green representing up- and down-regulation respectively. [score:10]
miR-144 (mmu-miR-144-3p) expression was much higher in type I lung epithelial cells than in CD45 [+] hematopoietic cells, whereas miR-451 (mmu-miR-451a) was expressed in both hematopoietic and epithelial cells (Fig 1A). [score:5]
This increased permissiveness for viral replication was not a generalized response to miRNA expression, since expression of miR-451 or miR-155 did not affect viral replication (Fig 2B and 2C). [score:5]
Therefore, to develop a mo del that matches the expression of miR-144/miR-451 in vivo, we generated lines of TC-1 and LET1 [14] cells stably over -expressing miR-144, miR-451, miR-155 (as a negative control), or vector alone (S4 Fig). [score:5]
A similar increase in viral load was observed when LET1 cells expressing miR-144 were compared with cells expressing miR-451. [score:4]
Expression of miR-144 and miR-451 in primary type I lung epithelial cells was compared to the expression level in primary polarized tracheal epithelial cells (mTEC), cultured primary lung alveolar epithelial type I cells (LET1), mouse TC-1 epithelial cell lines with or without stable transduction of microRNAs, and 293T cells. [score:4]
The expression of miR-144 and miR-451 in three tractable cell culture mo dels is significantly lower than in freshly isolated lung epithelial cells (S4 Fig). [score:3]
miR-451 alone was expressed with flanking sequences 100 bp upstream and 198 bp downstream. [score:3]
1006305.g003 Fig 3(A) Heat map depicting microarray analysis of influenza-infected TC-1 cells stably expressing miR-144+miR-451 or vector alone, with genes grouped by functional annotation. [score:3]
miR-144 and miR-451 are expressed in lung epithelial cells. [score:3]
To test this hypothesis, we generated immortalized lung type I epithelial cells with TRAF6 protein levels reduced by miR-144 or specific shRNAs, along with control cells expressing miR-451 or a non-functional shRNA (Fig 5A). [score:3]
miR-451 is adjacent to miR-144 on mouse chromosome 11 and both miRNAs are co-expressed in erythroid cells as one transcript that is processed into two mature miRNAs. [score:3]
Constructs expressing both murine mmu-miR-144-3p and mmu-miR-451a were cloned with 145 bp upstream of pre-miR-144 and 330 bp downstream from the end of pre-miR-451. [score:3]
Firefly/Renilla luminescence relative to cells expressing miR-451 for 4 independent experiments performed in triplicate are plotted (means ±SEM). [score:3]
1006305.g001 Fig 1(A) Expression of miR-144 and miR-451 in total lung cells and FACS-purified lung hematopoietic and epithelial cell populations were measured by qRT-PCR and plotted in arbitrary units relative to sno-202 expression. [score:3]
TRAF6 protein expression relative to actin was quantified by densitometry of Western blots: Uninfected: miR-451, 0.70; miR-144, 0.37; Infected: miR-451: 1.0; miR-144: 0.66. [score:3]
miR-451 was the most abundant miRNA with an available knockout mouse, which enabled us to functionally test the contribution of this miRNA to host response to influenza virus infection. [score:2]
miR-144 was cloned with 145 bp upstream of pre-miR-144 and 198 bp downstream of the end of pre-miR-451; the activity of miR-451 included in this construct was ablated using site-directed mutagenesis of 7 bp of the mature miR-451. [score:2]
Mean relative intensities for 5 (miR-144) or 2 (miR-451) independent experiments using 5 (vector alone) control samples are shown. [score:1]
Control shRNA, 1; TRAF6 shRNA, 0.47±0.12; miR-144, 0.68±0.09; miR-451, 1.16±0.26. [score:1]
Control shRNA, 1; TRAF6 shRNA, 0.43±0.15; miR-144, 0.52±0.12; miR-451, 0.79±0.12. [score:1]
Lung architecture was assessed to be normal in uninfected miR-144/miR-451 [null] mice. [score:1]
C57BL/6 mice (Jackson Laboratories), IRF7 [null] mice (C57BL/6 background, provided by T. Taniguchi, University of Tokyo, Tokyo, Japan), and miR-144/miR-451 [null] mice were housed in a specific pathogen-free barrier facility. [score:1]
Viral load in influenza-infected cells was quantified as in A. Means ±SEM for 3–7 independent experiments are shown and p-values calculated for miR-144+miR-451 and miR-144 -expressing cells relative to each other cell line. [score:1]
These data suggest that miR-144/miR-451 affects influenza virus replication in epithelial cells, as the largest difference in viral load was observed within the first 12 hours of infection, prior to substantial inflammatory cell recruitment. [score:1]
miR-144/miR-451 [null] mice [12] were backcrossed 5 times onto the C57BL/6 background (verified to be >95% C57BL/6), and wild type littermates used for infection experiments. [score:1]
We evaluated the effect of miR-144 and miR-451 on viral replication since they are expressed within the natural host cells for influenza [17– 19]. [score:1]
Means ± SEM are plotted for n = 5 (miR-144 and vector) or n = 2 (miR-451); *p = 0.013. [score:1]
miR-144 and miR-451 bind to unique sequences in target genes to play non-redundant roles in erythroid lineage differentiation [12, 15, 16] but are not well-characterized in the lung. [score:1]
[1 to 20 of 29 sentences]
8
[+] score: 70
Other miRNAs from this paper: mmu-mir-155, mmu-mir-451a
After 14 and 21 days, the effect of Mir-451 upregulation in erythroid differentiation was monitored by analyzing expression of transcriptional factor (Gata-1, Klf-1 and Epor) and hemoglobin chain (α, β, γ, ε and ζ) using quantitive reverse transcriptasePCR (qRT-PCR) and presence of erythroid cell surface markers (CD235a and Ter-119) using flow cytometry. [score:5]
An additional study on the expression profile of hemoglobin chains using qRT-PCR indicated that the up-regulation of Mir-451 induced a significant rise in mESC hemoglobinization and similarly we detected a sharp increase of accumulation of αglobin and β-globin transcripts in the pCDH-451 group. [score:5]
A. FACS histogram showing transduction efficiency of mESCs with lentiviral vector expressing pCDH-Mir-451, B. FACS histogram showing transduction efficiency of mESCs with lentiviral vector expressing pCDH-empty vector and C. FACS histogram showing transduction efficiency of untreated mESCs. [score:4]
Mir-451 plays an important role in promoting erythroid maturation, in part via its target GATA-2. As markers of erythropoiesis, we examined the expression of Gata-1, Epor, and Klf-1 transcription factors using qRT-PCR in all groups. [score:4]
Fig. 4Expression analysis (fold changes) of Mir-451 in treated murine embryonic stem cells (mESCs) on day 4. The expression of Mir-451 in the mESCs treated with pCDH-Mir-451 cells was significantly higher than that in mESCs treated with pCDH-empty vector and those untreated. [score:4]
revealed that these factors were expressed in mESCs transduced with lentiviral vector expressing pCDH- Mir-451. [score:4]
We show that Mir-451 up-regulation may play important roles in erythroid differentiation for in vitro erythropoiesis of mESCs and production of artificial RBCs without the presence of any stimulatory cytokines. [score:3]
Our results showed that Mir-451 up-regulation strongly induces erythroid differentiation and maturation of mESCs. [score:3]
Mir-451 up-regulation correlated with the induction of transcriptional factor (Gata-1, Klf-1, Epor) and hemoglobin chain (α, β, γ, ε and ζ) genes in mESCs (P<0.001) and also showed a strong correlation with presence of CD235a and Ter- 119 markers in these cells (13.084and 13.327-fold increse, respectively) (P<0.05). [score:3]
As shown in Table 2, in the pCDH-451-infected group, overexpression of Mir-451 led to a rise in the proportion of cells expressing TER119 and CD235a 30.12 ± 2.34% for and 17.47 ± 2.21%, respectively, compared with 3.87 ± 0.95% and 2.56 ± 0.87% of the control cells (untreated mESCs), respectively, on day 14 (7.782and 6.824-fold, respectively, P<0.05). [score:3]
FACS results indicated that Mir-451 up-regulation induced the erythroid surface markers TER119 and CD235a. [score:3]
In addition, they showed that Mir-451 is significantly up-regulated during erythroid differentiation. [score:3]
Lentiviruses expressing Mir-451 was then generated. [score:2]
We examined the effect of overexpression of Mir451 on erythroid differentiation of mESCs. [score:2]
Treatment of mESCs with pCDH-Mir-451 lentiviruses, led to the rise of Epor expression by 23.183-fold relative to the untreated mESCs on day 21 (P<0.001). [score:2]
In mESCs treated with pCDH- Mir-451 lentiviruses, mature Mir-451 expression level increased by 3.434-fold relative to the untreated mESCs (P<0.001, Fig. 4). [score:2]
Any expression changes of Mir-451 in murine erythroleukemia (MEL) cells promoted or impaired erythrocyte differentiation, respectively (23, 26). [score:2]
Overexpression of Mir-451 may have the potential to produce artificial red blood cells (RBCs) without the presence of any stimulatory cytokines. [score:2]
Therefore, Mir-451 seems to have more effect on the progression of erythroid maturation that increasing expression level of α-globin and β-globin. [score:2]
We determined the expression level of Mir-451 on day 4 after transduction in test and control groups by qRT-PCR. [score:2]
In our EB differentiation system, overexpression of Mir-451 in mESCs induced the differentiation of erythroid cells. [score:2]
Transduction efficiency and Mir-451 expression in murine embryonic stem cells. [score:2]
Mature Mir-451 expression level increased by 3.434-fold relative to the untreated mESCs on day 4 after transduction (P<0.001). [score:2]
In the mESCs treated with pCDH-Mir-451, Gata-1 and Klf-1 expression were increased by 1.952and 4.084-fold, respectively when compared with the untreated control group on day 14 (P<0.001) but was decreased by 0.712and 2.454-fold, respectively on day 21 (P<0.001). [score:1]
Recent studies have shown that specific miRNAs such as Mir-451 have key roles in erythropoiesis. [score:1]
Mir-451 and other miRNAs may be useful in designing effective therapeutic strategies for the possibility of reversing these abnormalities by gene therapy. [score:1]
In this experimental study, we examined the early stages of mESCs lineage commitment by investigating whether Mir-451 up-regulation could induce erythropoiesis differentiation from mESCs and be used as a replacement to the stimulatory cytokines for mESCs differentiation into erythroid cells. [score:1]
[1 to 20 of 27 sentences]
9
[+] score: 69
Considering the signaling pathway which induces the miRNA transcription directly upon LPS stimulation and suitable number of miRNA targets for biomarkers, expression of miRNAs in whole blood following LPS injection was quantified using real-time RT-PCR to verify selected up-regulated, but not down-regulated, miRNA targets with at least 4-fold increase in expression (let-7d, miR-15b, miR-16, miR-25, miR-92a, miR-103, miR-107, and miR-451). [score:16]
Upregulated expression of the miRNA targets (let-7d, miR-15b, miR-16, miR-25, miR-92a, miR-103, miR-107 and miR-451) following LPS injection on real-time RT-PCR was dose- and time -dependent. [score:8]
With a dose- and time -dependentupregulated expression of the miRNA targets (let-7d, miR-15b, miR-16, miR-25, miR-92a, miR-103, miR-107 and miR-451) following LPS injection, these whole blood-derived miRNAs are promising as biomarkers for LPS exposure. [score:8]
Expression of representative up-regulated miRNAs (let-7d, miR-15b, miR-16, miR-25, miR-92a, miR-103, miR-107, and miR-451) identified using miRNA microarray of whole blood using real-time RT-PCR. [score:6]
In contrast, LTA exposure induced moderate expression of miR-451 but not of the other 7 miRNA targets. [score:5]
In addition, following exposure to LPS, expression of 3 miRNAs (miR-15b, miR-16, and miR-451) was not significantly lower in TLR4 receptor knockout mice. [score:4]
The results showed that LTA only moderately induced miR-451 expression at concentrations of 100 and 1000 μg. [score:3]
In contrast, upon 100 ug and 1000 ug of LPS injection, all these 8 miRNAs (let-7d, miR-15b, miR-16, miR-25, miR-92a, miR-103, miR-107, and miR-451) had a significant expression than the control (Figure 2A). [score:3]
To investigate the role of the TLR4 receptor in inducing expression of the miRNA targets, expression of let-7d, miR-15b, miR-16, miR-25, miR-92a, miR-103, miR-107, and miR-451 in the whole blood of Tlr4 [−/−] mice 6 h after intraperitoneal injection of 100 μg LPS (L3755) was measured against that from the whole blood of Tlr4 [−/−] mice injected with PBS. [score:3]
Figure 4 Expression of let-7d, miR-15b, miR-16, miR-25, miR-92a, miR-103, miR-107, and miR-451 of whole blood from C57BL/6 and Tlr4 [−/−] (C57BL/10ScNJ) mice from real-time RT-PCR experiments 6 h after exposure to 100 μg LPS; **, P  < 0.01 vs. [score:3]
Figure 3 Expression of let-7d, miR-15b, miR-16, miR-25, miR-92a, miR-103, miR-107, and miR-451 from whole blood of C57BL/6 mice based on real-time RT-PCR experiments 6 h after exposure to 100 μg LPS originating from different bacteria, including Escherichia coli serotype 026:B6, Klebsiella pneumonia, Pseudomonas aeruginosa, Salmonella enterica, serotype Enteritidis, and Serratia marcescens. [score:3]
Figure 5 Expression of let-7d, miR-15b, miR-16, miR-25, miR-92a, miR-103, miR-107, and miR-451 of whole blood from C57BL/6 mice using real-time RT-PCR experiment 6 h after exposure to 10, 100, and 1000 μg LTA originating from Staphylococcus aureus ; *, P  < 0.05 vs. [score:3]
In this study, we demonstrated that expression of multiple miRNAs (let-7d, miR-15b, miR-16, miR-25, miR-92a, miR-103, miR-107, and miR-451) is significantly altered in the whole blood of mice after exposure to LPS in a dose- and time -dependent fashion. [score:3]
To investigate that whether lipoteichoic acid (LTA) originating from gram -positive bacteria induces expression of let-7d, miR-15b, miR-16, miR-25, miR-92a, miR-103, miR-107, and miR-451, whole blood was drawn at 6 h following intraperitoneal injections of 10, 100, or 1000 μg LTA from S. aureus for real-time PCR. [score:1]
[1 to 20 of 14 sentences]
10
[+] score: 45
The exosomes showed marked expression of 6 (miR-16, miR-17, miR-20a, miR-20b, miR-26a, and miR-26b) of the 10 miRNA targets at 8 h after CLP; the expression of the remaining 4 miRNA targets (miR-106a, miR-106b, miR-195, and miR-451) increased; however, the increase was not significant (Fig. 5B). [score:9]
The miRNA targets that were significantly up-regulated in the CLP experiment, as shown by the microarray experiments, are shown in Table 1. The expressions of 2 (miR-16 and miR-17), 6 (miR-20a, miR-16, miR-17, miR-451, miR-106a, and miR-106b), and 7 miRNAs (miR-26b, miR-20b, miR-17, miR-20a, miR-106a, miR-26a, and miR-195) increased significantly in the whole blood of mice at 4, 8, and 24 h after CLP, respectively. [score:8]
In this study, the mice with CLP experienced bacterial infection first and then septicemia, therefore, the results clearly showed that 8 miRNA targets (miR-16, miR-17, miR-20a, miR-26a, miR-26b, miR-106a, miR-106b, and miR-451) were up-regulated in both the CLP alone group and the E. coli infection group. [score:6]
Previously, we had demonstrated a dose- and time -dependent up-regulation of 8 (let-7d, miR-15b, miR-16, miR-25, miR-92a, miR-103, miR-107, and miR-451) and 4 (miR-451, miR-668, miR-1902, and miR-1904) circulating miRNA targets in mice following injection of LPS [11] and LTA [12], respectively. [score:6]
Although in some previous studies miR-16 and miR-142 showed relatively stable expression in the serum, owing to which these were used as endogenous controls [34], [35], studies have also shown that miR-16 and miR-451 expressed in red blood cells were the major source of variation in the estimated levels of circulating miR-16 and miR-451 [36]. [score:5]
These results show that 8 miRNAs (miR-16, miR-17, miR-20a, miR-26a, miR-26b, miR-106a, miR-106b, and miR-451) were up-regulated after both CLP and subcutaneous injection of E. coli. [score:4]
In this study, we demonstrated that experimental sepsis induced by CLP caused time -dependent upregulation of the circulating miRNAs miR-16, miR-17, miR-20a, miR-20b, miR-26a, miR-26b, miR-106a, miR-106b, miR-195, and miR-451. [score:4]
At 8 h after exposure injection, the level of 6 miRNAs (miR-451, miR-122, miR-350, miR-301a, miR-126, and miR-331) in the whole blood increased significantly. [score:1]
Among these miRNAs, the levels of miR-195 and miR-451 detected in the Ago2 immunoprecipitates were more than 20-fold that in the controls and the levels of miR-16, miR-20a, miR-26a, and miR-106b were more than 10-fold that in the control. [score:1]
Finally, miR-451 has been reported as a promising biomarker for Actinobacillus pleuropneumoniae infection in lung tissues [49]. [score:1]
[1 to 20 of 10 sentences]
11
[+] score: 35
xlsx”): Column 1: predicted target gene list used for GSEA; Column 2: subset list of predicted target genes present on microaarray; Column 3: leading edge subset of genes that were found to be either up or downregulated by comparing −H−D vs +H+D (normalized p value indicated on the top of the column); Column 4: leading edge subset gene list that were found to be either up or downregulated by comparing −H−D vs +H+D (normalized p value indicated on the top of the column); Column 5: intersection between leading edge gene lists in columns 3 and 4. Lists of leading edge common targets for miR-17 and miR-20 (intersection of the four gene lists in columns 3 and 4 on sheets miR-17 and miR-20), miR-19a and miR19b (intersection of the four gene lists in columns 3 and 4 on sheets miR-19a and miR-19b) as well as for miR-451 (intersection of gene lists in columns 3 and 4 in sheet miR-451) that have been used to generate the histograms presented in Figure 3B, C and D are given in sheet named «Gene list profile». [score:13]
As a control, target genes of miR-451, which is up-regulated in response to HMBA [36], tend in contrast to be over-represented among down-regulated genes. [score:9]
B: Mean relative expression profiles of the leading edge subsets of common predicted targets for miR-17/20a, miR-19a/19b and miR-451 identified by GSEA in response to progressive decrease of miR-17-92 expression or progressive increase of miR-451 induced by indicated combinations of HMBA and Dox treatment in 745A#44 cells. [score:7]
We also compared mean expression levels of genes in the leading edge subsets of common miR-17/miR-20a, common miR-19a/miR-19b and miR-451 targets identified in response to HMBA in the other two conditions (+Dox only or +HMBA only) which are associated with intermediate pri-miR-17-92 expression levels (Figure 1). [score:6]
[1 to 20 of 4 sentences]
12
[+] score: 31
Description miR-451[39] Upregulated in heart due to ischemia miR-22[40] Elevated serum levels in patients with stablechronic systolic heart failure miR-133[41] Downregulated in transverse aortic constrictionand isoproterenol -induced hypertrophy miR-709[42] Upregulated in rat heart four weeks after chronicdoxorubicin treatment miR-126[43] Association with outcome of ischemic andnonischemic cardiomyopathy in patients withchronic heart failure miR-30[44] Inversely related to CTGF in two rodent mo delsof heart disease, and human pathological leftventricular hypertrophy miR-29[45] Downregulated in the heart region adjacent toan infarct miR-143[46] Molecular key to switching of the vascular smoothmuscle cell phenotype that plays a critical role incardiovascular disease pathogenesis miR-24[47] Regulates cardiac fibrosis after myocardial infarction miR-23[48] Upregulated during cardiac hypertrophy miR-378[49] Cardiac hypertrophy control miR-125[50] Important regulator of hESC differentiation to cardiacmuscle(potential therapeutic application) miR-675[51] Elevated in plasma of heart failure patients let-7[52] Aberrant expression of let-7 members incardiovascular disease miR-16[53] Circulating prognostic biomarker in critical limbischemia miR-26[54] Downregulated in a rat cardiac hypertrophy mo del miR-669[55] Prevents skeletal muscle differentiation in postnatalcardiac progenitors To further confirm biological suitability of the identified miRNAs, we examined KEGG pathway enrichment using miRNA target genes (see ). [score:31]
[1 to 20 of 1 sentences]
13
[+] score: 31
Other miRNAs from this paper: mmu-mir-144, mmu-mir-34c, mmu-mir-34b, mmu-mir-34a, mmu-mir-451a
Overexpressed human mir-451 exhibited regulatory activity against its sensors in flies or fly cell lines. [score:4]
In fact, knockdown of Nibbler, the 3′→5′ exonuclease responsible for 3′-trimming of dAGO1 -loaded miRNAs derived from canonical miRNA duplexes (Han et al., 2011; Liu et al., 2011), surprisingly enhanced 3′-trimming of overexpressed miR-451 in fly cells. [score:4]
Artificial mir-451-like hairpins processed by Herpesvirus saimiri snRNAs integrator (Cazalla et al., 2011) or tRNase Z (Phizicky and Hopper, 2010) in a Drosha-independent manner can be processed into mature small RNAs loaded to Ago2 even in Drosha or Dicer knockout cells, providing proof-of-principle. [score:2]
Furthermore, although the natural mir-451 has a 5′ A, a mutant bearing a 5′ U had slightly enhanced activity against its targets compared to wild-type mir-451 (Yang et al., 2012). [score:2]
The mir-451 pathway was recently recognized to be present in flies (Yang et al., 2014). [score:1]
Although mir-451 precursor forms a hairpin structure, we will cover this miRNA in this review because the hairpin is not loaded as a duplex and, in theory, miR-451-like small RNAs could be generated in an RNase III-independent manner (see below). [score:1]
mir-451 is wi dely conserved in vertebrates, and its mutant mice exhibit defects in erythropoiesis (Patrick et al., 2010; Yu et al., 2010). [score:1]
mir-451 was originally found as a conserved hairpin located in a vicinity of a known miRNA mir-144 and was subsequently shown to associate with Ago2 (Altuvia et al., 2005; Nelson et al., 2007). [score:1]
Because the mir-451 hairpin has a highly paired stem region, Ago2 cleaves the 42 nt hairpin at the position complementary to 10th–11th nucleotides from the 5′ end of the hairpin, leaving a 30 nt half-hairpin (ac-pre-miRNA: Ago2-cleaved precursor miRNA). [score:1]
DICER-INDEPENDENT BIOGENESIS OF miR-451. [score:1]
To date, mir-451 is the only verified member of Dicer-independent, Drosha -dependent miRNAs. [score:1]
Further studies will be needed to see if the invertebrate mir-451 pathway and the RNase III-independent Ago2-loading pathway have any endogenous roles. [score:1]
Conserved vertebrate mir-451 provides a platform for Dicer-independent, Ago2 -mediated microRNA biogenesis. [score:1]
The resulting ac-pre-mir-451 (Ago2-cleaved-pre-miRNA: 30 nt) is further resected by the PARN exonuclease to mature as ~22–26 nt miR-451. [score:1]
The mir-451 hairpin is processed by Drosha–DGCR8 complex similar to canonical miRNAs (Figure 5A). [score:1]
The phenotypes could be partially rescued by a mir-451-like hairpin that was reprogrammed to produce mature species having the miR-430 sequence. [score:1]
Therefore, the removal of tails by PARN from ac-pre-mir-451-like molecules is not absolutely essential, although its minor contribution to miR-451 activity cannot be excluded. [score:1]
This suggested that Nibbler competes with the enzyme trimming ac-pre-mir-451 species (Yang et al., 2014). [score:1]
Although perfect pairing around the cleavage position and an unpaired 5′ nucleotide in the hairpin are important for maturation of mir-451-like hairpins, there appears to be no strict sequence restriction (Dueck et al., 2012; Yang et al., 2012). [score:1]
The 30 nt ac-pre-mir-451 is further resected by an exonuclease PARN to mature as ~22–26 nt species (Yoda et al., 2013). [score:1]
miR-451 protects against erythroid oxidant stress by repressing 14-3-3zeta. [score:1]
Instead of Dicer, the slicer activity of vertebrate Ago2 plays an essential role in mir-451 processing (Figure 5A). [score:1]
Defective erythroid differentiation in miR-451 mutant mice mediated by 14-3-3zeta. [score:1]
[1 to 20 of 23 sentences]
14
[+] score: 31
To confirm the time dependence of estrogen effect on miRNA expression in NZB/W [F1] mice, we analyzed the expression of miR-223 and miR-451, which were markedly upregulated by estrogen in wild-type B6 mice [42]. [score:8]
The expression of miR-223 and miR-451 in splenocytes was not increased with lupus manifestation in NZB/W [F1] mice (Figure S1) and the diversity in the expression level of select lupus -associated miRNAs in estrogen -treated mice with lymphoma development (Figure S2). [score:6]
Figure 5 Estrogen increased the expression of miR-223 and miR-451 expression in splenocytes from NZB/W [F1 ] mice. [score:5]
As expected, the expression levels of miR-223 and miR-451 were significantly upregulated in both 10-wk-old (Figure  5A) and 32-wk-old (Figure  5B) estrogen -treated mice when compared to age-matched intact or placebo -treated mice. [score:5]
Unlike lupus -associated miRNAs such as the miR-182 cluster that was highly increased in diseased, 36–40-wk-old NZB/W [F1] mice [34], miR-223 and miR-451 were not significantly increased in 36–40-wk-old female NZB/W [F1] mice when compared to pre-diseased NZB/W [F1] or NZW control (Additional file 1: Figure S1). [score:4]
The graphs show increased miR-223 and miR-451 expression in splenocytes from 10-wk-old (A) and 32-wk-old (B) estrogen -treated orchidectomized NZB/W [F1] mice when compared to either age-matched placebo control or intact control mice. [score:2]
This suggests that the remarkable increase of miR-223 and miR-451 in 32-wk-old estrogen -treated mice was attributable to estrogen effect, but not to lupus manifestation. [score:1]
[1 to 20 of 7 sentences]
15
[+] score: 25
These results indicate that CP2 binds to the core promoter of miR-144, induces the expression of mature miR-144 and miR-451, and eventually suppresses COX-2 expression and PGE2 production. [score:7]
[25] Paired box gene 4 (PAX4), which regulates human epithelial cancer metastasis, decreases miR-144 and miR-451 expression levels by binding to the promoter region of miR-144/451. [score:4]
[24] Here, we find that CP2 regulates the expression of miR-144 and miR-451 in mGCs, which is consistent with previous studies. [score:4]
23, 24, 25 We hypothesize that CP2 can also regulate miR-451 expression in mGCs. [score:4]
As shown in Figure 6b, CP2 significantly promoted miR-451 expression. [score:3]
There is increasing evidence that miR-144 and miR-451 are transcribed on a single primary RNA and regulated by same transcription factors. [score:2]
miR-144 and miR-451 are transcribed in the same pri-miRNA. [score:1]
[1 to 20 of 7 sentences]
16
[+] score: 25
In contrast, miR-451 was well expressed in precursors, but strongly down-regulated during differentiation (Cluster 5). [score:6]
We next verified changes in the expression of several miRNAs using quantitative RT-PCR (qRT-PCR), focusing on 3 miRNAs that had not been previously identified, to our knowledge, in cells of the osteoclast lineage: miR-99b-5p, miR-365-3p and miR-451. [score:3]
Expression of miR-451 decreased dramatically between 1 and 3 days of culture, such that it was virtually undetectable on days 3 or 5. 10.1371/journal. [score:3]
The expression of miR-365, miR-99b, and miR-451 was detected by qPCR in a MiQ qPCR cycler (Bio-Rad) and normalized to U6 small nuclear RNA (RNU6b) levels, using the absolute quantification method. [score:3]
Indeed, we could not detect expression of miR-451 by qRT-PCR in the bipotential mouse monocytic cell line RAW264.7 (data not shown). [score:3]
Expression of miR-451 decreased dramatically between 1 and 3 days of culture, such that it was virtually undetectable on days 3 or 5. 10.1371/journal. [score:3]
Therefore, it is possible that the high levels of miR-451 detected at day 1 are due to the presence of erythrocyte precursors in the cultures, which will not survive in culture with M-CSF and RANKL. [score:1]
It has been reported that miR-451 is required for erythroid differentiation and homeostasis [21], [22]. [score:1]
However, osteoclast number and size were not affected by the miR-451 mimic, suggesting that this miRNA may not have a significant role in osteoclastogenesis in vitro, although these data do not preclude potential actions in vivo (Figure 2C and D). [score:1]
Since miR-451 levels were dramatically decreased during osteoclast differentiation, to test its function, BMMs were transfected with a miR-451 mimic prior to RANKL -mediated differentiation. [score:1]
[1 to 20 of 10 sentences]
17
[+] score: 24
Comparing the inhibition of luciferase activity by the lentiviral expressed and endogenously expressed miRNAs, these results show that 1) the lentiviral expressed miR126 (both sense and antisense strands) and miR140 antisense strand exhibit potent RNAi activity; 2) the lentiviral expressed miR451 antisense strand does not have any RNAi activity; 3) the observed RNAi activity of lentiviral expressed miR21 (both sense and antisense strands) and miR140 sense strand could be due to endogenous miRNAs. [score:13]
Expression of the sense but not the antisense strand of gga-miR451 inhibited Renilla luciferase activity, consistent with the report from miRBase [23]. [score:5]
Based on literature reports and the miRNA database (miRBase), we chose four endogenous chicken miRNAs gga-miR21, gga-miR126, gga-miR140 and gga-miR451 that are expressed in many different tissues of adult chicken and chicken embryo [22]. [score:3]
Because gga-miR21, gga-miR126, gga-miR140 and gga-miR451 are generally expressed, we assayed their activity in DF-1 cells by directly transfecting the reporter plasmids into DF-1 cells. [score:3]
[1 to 20 of 4 sentences]
18
[+] 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]
[1 to 20 of 2 sentences]
19
[+] score: 19
Other miRNAs from this paper: hsa-mir-451a, mmu-mir-451a, hsa-mir-451b
The negative regulation of 14-3-3ζ by miR-451 has been elegantly demonstrated in breast cancer cells where it was shown that tamoxifen treatment leads to loss of miR-451 expression and up-regulation of 14-3-3ζ, correlating with increased disease severity [42]. [score:9]
Thus the reciprocal expression of miR-451 and 14-3-3ζ may be important prognostic markers for disease severity and cancer progression in NSCLC. [score:5]
Intriguingly, miR-451 expression has also been shown to be low in NSCLC tissue compared with non-cancerous lung tissue, and up-regulation of miR-451 in A549 cells reduced cell growth and increased the cells susceptibility to cisplatin [43]. [score:5]
[1 to 20 of 3 sentences]
20
[+] score: 18
Of these 15 miRNAs, we selected six miRNAs, miR-451, miR-126, miR-145, miR-146b-5p, miR-491-5p, and miR-107, which were previously reported to have a tumor suppressor role because our previous studies revealed that some tumor suppressor miRNAs in plasma were significantly down-regulated in cancer patients compared with healthy volunteers 30, 32, 33, and the down-regulation of tumor suppressor miRNAs in the blood stream might be related to tumor progression and poor prognostic outcomes [32]. [score:12]
We selected six down-regulated tumor suppressor miRNAs (miR-451, miR-126, miR-145, miR-146b-5p, miR-491-5p, and miR-107) in plasma through a comprehensive miRNA array -based approach. [score:6]
[1 to 20 of 2 sentences]
21
[+] score: 17
Most importantly, the predicted target genes for miRNAs also included the cytoskeleton remo delling protein tropomodulin (target for miR451) and Tm 1α and 2β, the latter of which is a molecule essential for maintaining structural biology of several organs including eye lens [53]. [score:5]
Of the latter, miR126, miR136, miR206, miR451 and miR551b showed significant, gradual down-regulation (>2 times) after birth or during development (ED16>4W>4W). [score:5]
In contrast, miR126 and miR-451 were significantly down-regulated (Fig. 2). [score:4]
Relative expression levels of miRNAs, let-7b, let-7c, miR-29a, miR-29c, miR-204, miR-126, miR-451 in ED16, 4W and 14W lenses are represented as histograms with normalized averages ± SD. [score:3]
[1 to 20 of 4 sentences]
22
[+] score: 17
In the non-alcoholic fatty liver disease mo del, the treatment with a dietetic regimen, which caused various liver injuries, demonstrated that there was significant downregulation of miR-451 and miR-27 in the livers of these rats 45. [score:6]
A significant increase of the expression of miR-15b and miR-451 was observed in C57BL/6 mice that received intraperitoneal injections of LPS 32. [score:3]
MiR-451 was reported to act as a “tuner” of gene expression related to erythroid homeostasis 43. [score:2]
These data demonstrated that miR-15b and miR-451 are involved in the development of liver inflammation. [score:2]
MiR-451 confers protection against simulated ischemia/reperfusion -induced cardiomyocyte death at least partly by targeting the CUG triplet repeat -binding protein 2- cyclooxygenase-2 (COX-2) pathway 44. [score:2]
These data suggest that miR-451 is involved in the anti-inflammatory response(s). [score:1]
Furthermore, in a mouse-to-rat cardiac xenotransplantation mo del, miR-451 in the grafts was lower, while miR-146a was higher than the isograft control at the endpoint of rejection 46. [score:1]
[1 to 20 of 7 sentences]
23
[+] score: 16
Other miRNAs from this paper: mmu-let-7g, mmu-let-7i, mmu-mir-23b, mmu-mir-27b, mmu-mir-126a, mmu-mir-127, mmu-mir-145a, mmu-mir-181a-2, mmu-mir-182, mmu-mir-199a-1, mmu-mir-122, mmu-mir-143, mmu-mir-298, mmu-let-7d, 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-23a, mmu-mir-27a, mmu-mir-31, mmu-mir-98, mmu-mir-181a-1, mmu-mir-199a-2, mmu-mir-181b-1, mmu-mir-379, mmu-mir-181b-2, mmu-mir-449a, mmu-mir-451a, mmu-mir-466a, mmu-mir-486a, mmu-mir-671, mmu-mir-669a-1, mmu-mir-669b, mmu-mir-669a-2, mmu-mir-669a-3, mmu-mir-669c, mmu-mir-491, mmu-mir-700, mmu-mir-500, mmu-mir-18b, 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-466d, 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-466j, mmu-mir-669e, 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-669a-4, mmu-mir-669a-5, mmu-mir-466c-2, mmu-mir-669a-6, mmu-mir-466b-4, mmu-mir-669a-7, mmu-mir-466b-5, mmu-mir-669p-1, mmu-mir-669a-8, mmu-mir-466b-6, mmu-mir-669a-9, mmu-mir-466b-7, mmu-mir-669p-2, mmu-mir-669a-10, mmu-mir-669a-11, mmu-mir-669a-12, mmu-mir-466p, mmu-mir-466n, mmu-mir-486b, mmu-mir-466b-8, mmu-mir-466q, mmu-mir-145b, mmu-let-7j, mmu-let-7k, mmu-mir-126b, mmu-mir-466c-3
For example, miR-127 has been shown to participate in cancer development [85], miR-145 has been shown to control c-Myc expression through p53 [86], miR-199a regulates MET protooncogene and affects NF-KB expression [54], miR-379 affects brain neuronal development [87], [88], miR-451 affects erythroid differentiation [89], miR-126 affects angiogenic signaling and controls blood vessel development [90], miR-143 regulates ERK5 signaling and targets KRAS gene [91], miR-298 regulates CYPA3 expression [92] and miR-486 regulates kinase activity and tumor progression [93]. [score:16]
[1 to 20 of 1 sentences]
24
[+] score: 16
Next, real-time PCR was performed to further validate the differentially expressed miRNAs after H. pylori infection in MKN45 cells for 12 h and 24 h. The results showed that, all the miRNAs including miR-29b-1, miR-3125, miR-30a-3p, miR-340, miR-301a, and miR-451 showed decreased expression of varying levels, and the downregulation of miR-30a-3p expression was particularly notable (Fig.   1C). [score:10]
Further systematical analysis demonstrated that, miR-29b-1, miR-3125, miR-30a-3p, miR-340, miR-301a and miR-451 were the most significantly down-regulated miRNAs that target the COX-2 gene in H. pylori-infected MKN45 cells (Fig.   1A,B). [score:6]
[1 to 20 of 2 sentences]
25
[+] score: 14
Other miRNAs from this paper: mmu-mir-144, mmu-mir-322, mmu-mir-451a, mmu-mir-503
miR-451 displayed clear “blood islands” staining with the X-gal/FeCN method, which suggests that miR-451 has relatively high expression at E8.5 (Fig 6A). [score:3]
0176915.g006 Fig 6Verification of the improved method in E8.5 miR-451- LacZ embryos. [score:1]
The improved method is applicable for other LacZ reportersWe used another LacZ reporter strain, miR-451 promoter- LacZ, to test if the new method is broadly applicable. [score:1]
The E8.5 miR-451 promoter- LacZ embryos were generated from mating between transgenic male miR-451 promoter- LacZ mice and wildtype female SW mice. [score:1]
Verification of the improved method in E8.5 miR-451- LacZ embryos. [score:1]
At E8.5, miR-451 is localized in the yolk sac “blood islands”, which further differentiate into erythrocytes [16]. [score:1]
In conclusion, the improved method showed not only specific staining similar as the staining from X-gal/FeCN method but also more staining details, which may indicate miR-451’s function in other parts of E8.5 mouse embryos. [score:1]
According to previous reports, miR-451 is important for erythropoiesis under oxidative stress [18]. [score:1]
We used another LacZ reporter strain, miR-451 promoter- LacZ, to test if the new method is broadly applicable. [score:1]
The miR-451 promoter- LacZ is a transgenic mouse strain with the LacZ gene under the control of the 5-kb promoter of miR-144/451 [16]. [score:1]
miR-451 promoter- LacZ positive embryos were obtained by mating male transgenic miR-451 promoter- LacZ mice with wildtype female SW mice. [score:1]
E8.5 miR-451 promoter- LacZ positive embryos were produced from the mating between heterozygous male miR-451 promoter- LacZ mice and wildtype SW female mice. [score:1]
[1 to 20 of 12 sentences]
26
[+] score: 14
Some differentially expressed miRNAs in liver had important functions, such as involvement in nutrient metabolism, including a cholesterol metabolism regulator (miR-122), a lipid metabolism regulator (miR-705), an adipocyte differentiation and regulation factor (miR-27a and miR-193), and erythrocyte differentiation (miR-223 and miR-451). [score:6]
Given that the main food resource of schistosomes is the erythrocyte of the host, the higher expression level of miR-223 and the lower expression level of miR-451 might affect the quality and quantity of the erythrocyte from M. fortis, which could in turn reduce the food resource of schistosome. [score:5]
miR-451 is a key molecule that regulates erythroid differentiation in vivo, and the lack of miR-451 might decrease the hematocrit of mice [37]. [score:2]
MiR-122, miR-451 and miR-494 were detected in liver, miR-494, miR-691 and miR-143 in spleen, and miR-223, miR-200a and miR-322 in lung. [score:1]
[1 to 20 of 4 sentences]
27
[+] score: 14
The expression analysis revealed a number of miRNAs that previously have not been demonstrated to be highly expressed in the lung, including miR-451 (Figure 2). [score:5]
MiR-451 is genomically located at mouse chromosome 11 B5 and the syntenic region at human chromosome 17q11.2, and is expressed in both species from an intergenic region upstream of miR-144 (miR-144 was not available as part of the RT-PCR miRNA expression panel). [score:5]
Foregoing research indicated that miR-451 may be involved in the specific differentiation of erythrocytes [26], although such high expression in lung tissue suggests that alternative cell types, such as pulmonary epithelial cells, require miR-451 for their maintenance and/or development. [score:4]
[1 to 20 of 3 sentences]
28
[+] score: 14
In contrast to miR-451 locus whose expression was restricted to the fetal liver in embryonic day (E) 16.5 mouse embryos, the major site of haematopoiesis and erythropoiesis at this stage of development, miR-27a and miR-24 seem to serve as universal regulators in different cell types. [score:5]
Meanwhile, Dore et al. (6) found that dre-miR-451 could modulate zebrafish erythrocyte maturation via targeting gata-2. Their observations suggested the existing of a GATA-1/miR-451/GATA-2 axis in mouse and zebrafish erythropoiesis, although needs further validation. [score:3]
So far, a number of non-coding regulators such as miR-451 (5, 6), miR-23a (7), miR-221/222 (8), miR-376a (9) and miR-223 (10) were reported to play positive or negative roles in controlling erythropoiesis. [score:2]
Despite the fact that miR-451, miR-23a and mir-223 were shown to suffer from GATA-1 regulation in some species (6, 7, 11), there are virtually no data about GATA-1/2 switch dynamically operating on their genes during erythropoiesis. [score:2]
In mouse erythroid cells, GATA-1 was demonstrated to positively regulate a previously identified mmu-miR-451 (5). [score:2]
[1 to 20 of 5 sentences]
29
[+] score: 10
Upregulation of miR-451 expression inactivates the AKT signaling pathway and enhanced cisplatin induced apoptosis in A549 cells [17]. [score:6]
For instance, miR-451 is downregulated in NSCLC tissues and is capable of conferring resistance to cisplatin in non-small cell lung cancer cell line (A549) [40]. [score:4]
[1 to 20 of 2 sentences]
30
[+] score: 9
Other miRNAs from this paper: mmu-mir-122, mmu-mir-451a
It was reported [24] that miR-451 negatively regulates LKB1 activity by binding directly to a 3′-untranslated region of MO25 mRNA and suppressing its expression. [score:9]
[1 to 20 of 1 sentences]
31
[+] score: 9
Other miRNAs from this paper: mmu-mir-155, mmu-mir-451a, rno-mir-451, rno-mir-155
[18] The absence of the passenger strand from the miR-451 scaffold provides a better safety profile for therapeutic shRNAs or miRNAs since it reduces the chance for off-target suppression of other genes by the passenger strand. [score:5]
In this study, we showed that the miHTT construct processed from the miR-451 scaffold is able to strongly suppress mutant HTT aggregation and ultimately dramatically reduce the generation of striatal lesions at two months post-injection. [score:3]
We did not observe any reads belonging to the passenger strand, confirming the absence of a passenger strand associated with the miR-451 precursor. [score:1]
[1 to 20 of 3 sentences]
32
[+] score: 9
Other miRNAs from this paper: mmu-let-7i, hsa-let-7i, hsa-mir-451a, mmu-mir-451a, hsa-mir-451b
Downstream, miR-451 appears to fuse with transcripts of the regulatory subunit of the parasite's cAMP -dependent protein kinase (PKA-R) to reduce its translation, thereby upregulating activity of its substrate PKA and ultimately disrupting multiple parasite developmental pathways. [score:8]
Specifically, the host miRNAs miR-451 and let-7i were significantly more abundant in HbAS and HbSS RBCs, and were associated with attenuated parasite growth in these cells. [score:1]
[1 to 20 of 2 sentences]
33
[+] score: 8
MiR-451, which was over-expressed in SP-HCCs, is involved in activating the expression of P-glycoprotein (P-gp), the MDR1 gene product that confers the SP phenotype [54]. [score:4]
Among the moderately up-regulated miRNAs, miR-451 and miR-181a have been well studied. [score:4]
[1 to 20 of 2 sentences]
34
[+] score: 8
The highest dysregulated miRNAs identified in the cMyBP-C related HCM mo del were the miR-192 and miR-429 for the upregulated, and the miR-451 and miR-301a for the downregulated. [score:8]
[1 to 20 of 1 sentences]
35
[+] score: 7
Oncomirs specifically expressed in tumor samples at the highest expression level included miR-106a, miR-17, miR-454, let-7e, miR-451, miR-886-5p, miR-601 and miR-625 (expression score of ≥2, Figure 5A). [score:7]
[1 to 20 of 1 sentences]
36
[+] score: 7
Figure 1A shows that 30 miRNAs were significantly modulated by more than two-fold, within these seven miRNAs were upregulated (let-7d, life-26-3p, miR-16, miR-451, miR-486-5p, miR-518e*, miR-720) and twenty one were downregulated. [score:7]
[1 to 20 of 1 sentences]
37
[+] score: 7
Svasti S. Masaki S. Penglong T. Abe Y. Winichagoon P. Fucharoen S. Umemura T. Expression of microRNA-451 in normal and thalassemic erythropoiesis Ann. [score:3]
Another in vivo study confirmed that miR-451 played a positive role in the regulation of erythroid maturation in erythroid-differentiating K562 cells [54]. [score:2]
Bruchova-Votavova H. Yoon D. Prchal J. T. miR-451 enhances erythroid differentiation in K562 cells Leuk. [score:1]
However, an in vitro study showed that only miR-451 had functions in zebrafish erythropoiesis [23]. [score:1]
[1 to 20 of 4 sentences]
38
[+] score: 7
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-21, hsa-mir-22, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26a-1, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-99a, mmu-let-7g, mmu-let-7i, mmu-mir-27b, mmu-mir-99a, mmu-mir-140, mmu-mir-10b, mmu-mir-181a-2, mmu-mir-24-1, mmu-mir-191, hsa-mir-192, hsa-mir-148a, hsa-mir-30d, mmu-mir-122, hsa-mir-10b, hsa-mir-181a-2, hsa-mir-181a-1, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-122, hsa-mir-140, hsa-mir-191, hsa-mir-320a, mmu-mir-30d, mmu-mir-148a, mmu-mir-192, 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-21a, mmu-mir-22, mmu-mir-24-2, mmu-mir-26a-1, mmu-mir-92a-2, mmu-mir-25, mmu-mir-181a-1, mmu-mir-26a-2, mmu-mir-92a-1, hsa-mir-26a-2, hsa-mir-423, hsa-mir-451a, mmu-mir-451a, hsa-mir-486-1, mmu-mir-486a, mmu-mir-423, bta-mir-26a-2, bta-let-7f-2, bta-mir-148a, bta-mir-21, bta-mir-30d, bta-mir-320a-2, bta-mir-99a, bta-mir-181a-2, bta-mir-27b, bta-mir-140, bta-mir-92a-2, bta-let-7d, bta-mir-191, bta-mir-192, bta-mir-22, bta-mir-423, bta-let-7g, bta-mir-10b, bta-mir-24-2, bta-let-7a-1, bta-let-7f-1, bta-mir-122, bta-let-7i, bta-mir-25, bta-let-7a-2, bta-let-7a-3, bta-let-7b, bta-let-7c, bta-let-7e, hsa-mir-1246, bta-mir-24-1, bta-mir-26a-1, bta-mir-451, bta-mir-486, bta-mir-92a-1, bta-mir-181a-1, bta-mir-320a-1, mmu-mir-486b, hsa-mir-451b, bta-mir-1246, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-let-7k, hsa-mir-486-2
There were eight microRNAs (bta-miR-27b, bta-miR-191, bta-miR-30d, bta-miR-451, bta-miR-25, bta-miR-140, bta-miR-24-3p, and bta-miR-122), that were upregulated in older animals in the present study, and upregulated in fetal muscle tissue of the study. [score:7]
[1 to 20 of 1 sentences]
39
[+] score: 7
Sun Y miR-451 suppresses the NF-kappaB -mediated proinflammatory molecules expression through inhibiting LMP7 in diabetic nephropathyMol. [score:7]
[1 to 20 of 1 sentences]
40
[+] score: 7
Reduction of p300 mRNA was concomitant with increased expression of mmu-miR-451 and mmu-miR-363 that targets 3’-UTR of p300. [score:5]
Mmu-miR-451 is known to destabilize cytokine mRNAs [21] and mmu-miR-363 is known to be associated with regulation of MAPK signaling [22]. [score:2]
[1 to 20 of 2 sentences]
41
[+] score: 7
In this study, we demonstrated the expression of SM miRNAs was reduced by 87% in the KO SMCs: 136 miRNAs were not detectable, 222 miRNAs were reduced with >2 fold, and 26 miRNAs including miR-451 were upregulated with >2 fold (Table 2; details in Table S2). [score:6]
Recent studies showed that miR-451 is indeed processed by Dicer-independent Ago2 [40], [41]. [score:1]
[1 to 20 of 2 sentences]
42
[+] score: 7
The increased expression of mml-miR-451 and mml-miR-144 in the skeletal muscle of old rhesus monkey is reversed by CR [17], but in our study, we did not see any significant effect of CR on the expression of mmu-miR-451, whereas expression of mmu-miR-144 was below the detection threshold. [score:7]
[1 to 20 of 1 sentences]
43
[+] score: 7
In contrast, another seven miRNAs (miR-126-3p, miR-23b, miR-27a, miR-29a, miR-29c, miR-451, and miR-690) were significantly up-regulated in the liver but down-regulated in the brain. [score:7]
[1 to 20 of 1 sentences]
44
[+] score: 7
The comparison between control- and MPA -treated cells revealed that 16 miRNAs were significantly modulated by more than two-fold (P < 0.05, Figure 1A), nine miRNAs were upregulated (miR-191*, miR-17*, miR- 470*, miR-451, miR-702, miR-434-3p, miR-493, miR-23a* and miR-485*) and seven were downregulated (miR-378*, miR-376a, miR-224, miR-190b, miR-16, miR-410 and miR-197) (Figure 1B). [score:7]
[1 to 20 of 1 sentences]
45
[+] score: 7
For example, miR-451, one of the 11 miRNAs we found modulated in the HD monkeys, is also upregulated in HD patients [24]. [score:4]
However, miR-451 does not appear to be disrupted in HD mice mo dels, suggesting the involvement of this miRNA in disease progression may be restricted to primates. [score:3]
[1 to 20 of 2 sentences]
46
[+] score: 6
For example, evolutionarily conserved sequences such as miR-451 and miR-150 are highly expressed in bone marrow [15], regulating hematopoiesis, and miR-126 and let-7 family members show high expression in lung [16, 17]. [score:6]
[1 to 20 of 1 sentences]
47
[+] score: 6
Other miRNAs from this paper: mmu-mir-451a
In this study, the authors reported that by targeting the mir-451 -mediated activation of the PI3K/mTOR/Akt pathway with inhibitors Rapamycin and S14161, the myeloma CSC population was directly reduced via apoptosis [4]. [score:6]
[1 to 20 of 1 sentences]
48
[+] score: 6
miR-434-5p - ND miR-451 +miR-451 expression was up-regulated in multidrug resistant cancer cell lines [58]. [score:6]
[1 to 20 of 1 sentences]
49
[+] score: 6
Several studies have shown that many miRNAs, such as miR-155 and miR-451, were dysregulated in the synovial membrane and regulated the inflammatory response in clinical or experimental arthritis [28– 31]. [score:3]
Murata K Yoshitomi H Furu M Ishikawa M Shibuya H Ito H Matsuda S MicroRNA-451 down-regulates neutrophil chemotaxis via p38 MAPKArthritis Rheum. [score:3]
[1 to 20 of 2 sentences]
50
[+] score: 6
Only five miRNAs (mmu-miR-451, mmu-miR-223, mmu-miR-92a, mmu-miR-200c, and mmu-miR-873) were differentially expressed, implying that the majority of miRNA downregulation associated with obesity could be reversed by LFD treatment. [score:6]
[1 to 20 of 1 sentences]
51
[+] score: 6
Other miRNAs from this paper: mmu-mir-451a
Peng Z, Zhang Y. Propofol inhibits proliferation and accelerates apoptosis of human gastric cancer cells by regulation of microRNA-451 and MMP-2 expression. [score:6]
[1 to 20 of 1 sentences]
52
[+] score: 6
Other miRNAs from this paper: mmu-mir-122, hsa-mir-122, hsa-mir-451a, mmu-mir-451a, hsa-mir-451b
This intrinsic slicing ability also plays a crucial role during the biogenesis of certain cellular miRNAs, as evidenced by reduced baseline expression of mature miRNAs in Ago2 knockout cells (26, 27), or Ago2-cleaved precursor (ac-pre-)miRNAs and Ago2 -dependent Dicer-independent processing of miR-451 (26, 28–30). [score:4]
In the future, it will be interesting and informative to more thoroughly investigate whether these dose -dependent Ago2 saturation effects coincide with dysregulated miRNA expression and/or functionality, considering the aforementioned recent findings of Ago2 -dependent processing of individual miRNAs, such as miR-451(26, 28–30). [score:2]
[1 to 20 of 2 sentences]
53
[+] score: 6
Upregulation of miR-2861 and miR-451 expression in papillary thyroid carcinoma with lymph node metastasis. [score:6]
[1 to 20 of 1 sentences]
54
[+] score: 6
It is worth noting that in general the entire pattern of upregulated tumour-derived miRNAs is not unambiguous because we observed the activation of both tumour-suppressor (miRNAs of let-7 family, mir-451) and oncogenic miRNAs (mir-29b, mir-21). [score:6]
[1 to 20 of 1 sentences]
55
[+] score: 5
Decreased miR-144 and miR-451 were found in NASH, where the former elicits and the latter inhibits proinflammatory cytokine production by respectively targeting TLR-2 [29]and AMPK/AKT pathway [30]. [score:5]
[1 to 20 of 1 sentences]
56
[+] score: 5
Validation by quantitative PCR (qPCR) confirmed that the expression levels of miR-182, miR-223, and miR-142-3p in the HRT users were approximately one-third of that of nonusers (P = 0.05, 0.001 and 0.003, respectively; Fig. 1C), while miR-142-5p and miR-451 were not significantly different between HRT users and their nonuser co-twins. [score:3]
MiR array data showed miR-142-3p, miR-142-5p, miR-223, miR-182, and miR-451 to be hypo-expressed in the HRT users compared to nonusers (Fig. 1B). [score:2]
[1 to 20 of 2 sentences]
57
[+] score: 5
Other miRNAs from this paper: hsa-mir-25, mmu-mir-25, hsa-mir-451a, mmu-mir-451a, hsa-mir-451b
Reversely, AMPK inhibition, for example via expressing microRNA-451, could promote CRC cell proliferation and progression [10]. [score:5]
[1 to 20 of 1 sentences]
58
[+] score: 5
Instead, pre-miR-451 is directly loaded onto RISC, where AGO2 -dependent cleavage generates ac-pre-miR-451 (AGO-cleaved pre-miR-451) (Cheloufi et al., 2010; Cifuentes et al., 2010; Yang et al., 2010). [score:2]
Thereafter, the poly(A)-specific ribonuclease (PARN) further trims the 3′ end of ac-pre-miR-451 to generate mature versions of miR-451 harboring divergent 3′ ends (Yoda et al., 2013). [score:1]
Drosha -dependently processed pre-miR-451 has a stem of only ~18 bp, which is too short for Dicer -mediated cleavage. [score:1]
A Dicer-independent biogenesis pathway was also recently reported for a miRNA, as the maturation of miR-451 was shown to require Drosha but not Dicer (Cheloufi et al., 2010; Cifuentes et al., 2010; Yang et al., 2010). [score:1]
[1 to 20 of 4 sentences]
59
[+] score: 5
They found that miR-320, miR-378, miR-211, miR-200a,b and miR-184 were significantly down-regulated during both stages of hibernation compared with non-hibernating animals, whereas miR-486, miR-451, miR-144 and miR-142 were significantly overexpressed in late torpor phase [22]. [score:5]
[1 to 20 of 1 sentences]
60
[+] score: 4
It is notable that AGO2 is capable of processing certain miRNAs without Dicer, including miR-451 [35], [36], and miR-451 was among the few upregulated miRNAs in TLE-HS tissue. [score:4]
[1 to 20 of 1 sentences]
61
[+] score: 4
Zhu H. Wu H. Liu X. Evans B. R. Medina D. J. Liu C. G. Yang J. M. Role of microRNA miR-27a and miR-451 in the regulation of MDR1/P-glycoprotein expression in human cancer cells Biochem. [score:4]
[1 to 20 of 1 sentences]
62
[+] score: 4
Other miRNAs from this paper: hsa-mir-451a, mmu-mir-451a, hsa-mir-451b
Of the 11 miRNAs that may interact with PGC-1α, mir-451 is predicted to interact with mtDNA in the mitochondrial matrix and has been shown to be up-regulated in individuals who fail to generate increased muscle mass in response to resistance training [40- 42]. [score:4]
[1 to 20 of 1 sentences]
63
[+] score: 4
In addition, the results seemed to contrast to our previous report that LPS injection induced up-regulation of the miRNAs (let-7d, miR-15b, miR-16, miR-25, miR-92a, miR-103, miR-107 and miR-451) of the whole blood in a dose- and time -dependent manner [19]. [score:4]
[1 to 20 of 1 sentences]
64
[+] score: 4
Other miRNAs, such as miR-27a, miR-29b, miR-125a, miR-146a, miR-122, miR-181a, miR-204-5p and miR-451 are differentially up-regulated in M1 and M2 spectrum macrophages [45, 46]. [score:4]
[1 to 20 of 1 sentences]
65
[+] score: 4
MiR-451 was differentially expressed in the livers of infected animals, which suggests that erythroid differentiation may be altered following S. japonicum infection [36, 37]. [score:2]
It was found that miR-494, miR-365 and miR-451 were present in liver, miR-206, miR-468 and miR-691 in spleen, and miR-223, miR-98 and miR-206 in lung. [score:1]
33rno-miR-19b−1.590.33rno-miR-451−4.370.05rno-miR-196c*−1.660.32Tissue/LungLog2(infected/control)Fold changemmu-miR-32*−2.170.22rno-miR-2062.234.69mmu-miR-328*−2.630.16rno-miR-2231.823.53rno-miR-32*−2.850.14rno-miR-981.22.3mmu-miR-468−3.490.09mmu-miR-4681.192.28mmu-miR-691−4.040.06mmu-miR-669d1.112.16mmu-miR-297a−4.620.04rno-miR-328a*1.12.14mmu-miR-467h−4.960. [score:1]
[1 to 20 of 3 sentences]
66
[+] score: 4
Differences between groups were lower in the adipocyte fraction, with miR-451 (1.8-fold, p<0.05) and -486 (1.7-fold, p<0.05) being modestly upregulated. [score:4]
[1 to 20 of 1 sentences]
67
[+] score: 4
Another Dicer-independent pathway is observed for the mir-451 family, this pathway involves the catalytic activity of the Ago2 protein [38– 40]. [score:1]
The data on Fig.   1a includes the canonical miRNAs, Drosha-independent mirtrons and a small number of other non-canonical miRNAs, e. g. Dicer-independent mir-451 family [29], simtrons [37], etc. [score:1]
The mir-451 family can be processed by the canonical pathway as well as by the non-canonical one in which Drosha produces a short hairpin with the miRNA that overlaps within the terminal loop. [score:1]
Drosha generates pre-mir-451 with ~ 18-nt stem which is too short to be processed by Dicer. [score:1]
[1 to 20 of 4 sentences]
68
[+] score: 4
At 16 months, all 15 miRNAs were significantly downregulated in heart tissue of obese mice compared to heart tissue of normal mice: let-7f-5p (FC: 3.3), miR-10a-5p (FC: 2.6), miRNA-19b-3p (FC: 5.0), miR-25-3p (FC: 2.6), miR30e-5p (FC: 5.6), miR-140-5p (FC: 5.0), miR-155-5p (FC: 1.7), miR-146a-5p (FC: 4.0), miR-181b-5p (3.0), miR-199a-3p (FC: 3.6), miR-322 (FC: 1.5), miR-451 (FC: 1.9), miR-499-5p (FC: 5.4), miR-669m-5p (FC: 1.7) and miR-3473b (FC: 3.4). [score:3]
Based on previous pre-clinic studies, the miRNAs validated by RT-qPCR in our study are involved in alteration of glucose and lipid metabolism via insulin pathways (let-7f-5p, miR-10a-5p, miR-322) 20– 22, in cardiomyocytes apoptosis (miR-19b-3p, miR-25-3p, miR-30e-5p, miR-140-5p, miR-199a-3p, miR-499) 23– 28, in mitochondrial function (miR-181a/b) [29], in pro-inflammatory signalling (miR-146a-5p, miR-155, miR-181b-3p, miR-3473b) 30– 33, and in cardiac hypertrophy (miR-451) [34] and myocardial fibrosis process (miR-19b) 35, 36. [score:1]
[1 to 20 of 2 sentences]
69
[+] score: 4
Other miRNAs from this paper: hsa-mir-451a, mmu-mir-451a, hsa-mir-451b
In addition, Andriani et al [46] showed increased sensitivity to cisplatin after applying a FHIT gene into the NSCLC cells, and Bian et al [47] reported increasing cisplatin sensitivity of NSCLC cells by up-regulation of miRNA451. [score:4]
[1 to 20 of 1 sentences]
70
[+] score: 3
Mir-451 and mir-340-5p, which were shown to be up regulated in the brain post TBI, were down regulated in our experiment [19], [61]. [score:3]
[1 to 20 of 1 sentences]
71
[+] score: 3
Moreover, microRNA-451 induces EMT in docetaxel-resistant lung adenocarcinoma cells by targeting proto-oncogene c-Myc [41]. [score:3]
[1 to 20 of 1 sentences]
72
[+] score: 3
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-16-1, hsa-mir-17, hsa-mir-21, hsa-mir-22, hsa-mir-28, hsa-mir-29b-1, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-29b-1, mmu-mir-124-3, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-145a, mmu-mir-150, mmu-mir-10b, mmu-mir-195a, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, mmu-mir-206, mmu-mir-143, hsa-mir-10a, hsa-mir-10b, hsa-mir-199a-2, hsa-mir-217, hsa-mir-218-1, hsa-mir-223, hsa-mir-200b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-143, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-150, hsa-mir-195, hsa-mir-206, 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-16-1, mmu-mir-16-2, mmu-mir-21a, mmu-mir-22, mmu-mir-29c, rno-let-7d, rno-mir-329, mmu-mir-329, rno-mir-331, mmu-mir-331, rno-mir-148b, mmu-mir-148b, rno-mir-135b, mmu-mir-135b, hsa-mir-200c, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-10a, mmu-mir-17, mmu-mir-28a, mmu-mir-200c, mmu-mir-218-1, mmu-mir-223, mmu-mir-199a-2, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-7b, mmu-mir-217, hsa-mir-29c, hsa-mir-200a, hsa-mir-365a, mmu-mir-365-1, hsa-mir-365b, hsa-mir-135b, hsa-mir-148b, hsa-mir-331, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, 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-7b, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-10a, rno-mir-10b, rno-mir-16, rno-mir-17-1, rno-mir-21, rno-mir-22, rno-mir-28, rno-mir-29b-1, rno-mir-29c-1, rno-mir-124-3, rno-mir-124-1, rno-mir-124-2, rno-mir-133a, rno-mir-143, rno-mir-145, rno-mir-150, rno-mir-195, rno-mir-199a, rno-mir-200c, rno-mir-200a, rno-mir-200b, rno-mir-206, rno-mir-217, rno-mir-223, dre-mir-7b, dre-mir-10a, dre-mir-10b-1, dre-mir-217, dre-mir-223, hsa-mir-429, mmu-mir-429, rno-mir-429, mmu-mir-365-2, rno-mir-365, dre-mir-429a, hsa-mir-329-1, hsa-mir-329-2, hsa-mir-451a, mmu-mir-451a, rno-mir-451, dre-mir-451, 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-9-1, dre-mir-9-2, dre-mir-9-4, dre-mir-9-3, dre-mir-9-5, dre-mir-9-6, dre-mir-9-7, dre-mir-10b-2, dre-mir-16a, dre-mir-16b, dre-mir-16c, dre-mir-17a-1, dre-mir-17a-2, dre-mir-21-1, dre-mir-21-2, dre-mir-22a, dre-mir-22b, dre-mir-29b-1, dre-mir-124-1, dre-mir-124-2, dre-mir-124-3, dre-mir-124-4, dre-mir-124-5, dre-mir-124-6, dre-mir-133a-2, dre-mir-133a-1, dre-mir-133b, dre-mir-133c, dre-mir-143, dre-mir-145, dre-mir-150, dre-mir-200a, dre-mir-200b, dre-mir-200c, dre-mir-206-1, dre-mir-206-2, dre-mir-365-1, dre-mir-365-2, dre-mir-365-3, dre-let-7j, dre-mir-135b, rno-mir-1, rno-mir-133b, rno-mir-17-2, mmu-mir-1b, dre-mir-429b, rno-mir-9b-3, rno-mir-9b-1, rno-mir-9b-2, rno-mir-133c, mmu-mir-28c, mmu-mir-28b, hsa-mir-451b, mmu-mir-195b, mmu-mir-133c, mmu-mir-145b, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-let-7k, rno-let-7g, rno-mir-29c-2, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
Cortex let-7c-1, miR-10a, miR-21, miR-124a-1, miR-128a, miR-135b, miR-150, miR-199a, miR-217, miR-329, miR-451. [score:1]
Olfactory bulb let-7b, let-7c-1, let-7c-2, miR-10a, miR-16, miR-17, miR-21, miR-22, miR-28, miR-29c, miR-124a-1, miR-124a-3, miR-128a, miR-135b, miR-143, miR-148b, miR-150, miR-199a, miR-206, miR-217, miR-223, miR-29b-1, miR-329, miR-331, miR-429, miR-451. [score:1]
Dorsal root ganglion let-7c, miR-17, miR-145, miR-150, miR-199a, miR-223, miR-365, miR-451. [score:1]
[1 to 20 of 3 sentences]
73
[+] score: 3
One that is expressed in red blood cells (miRNA-451), and one that is relatively stable in serum and plasma and not affected by hemolysis (miRNA-23a). [score:3]
[1 to 20 of 1 sentences]
74
[+] score: 3
For example, the unusual Dicer-independent locus mir-451 obligately depends on slicing by Ago2 for its maturation [15– 17], and this miRNA is one of the top-expressed miRNAs in erythrocytes [18]. [score:3]
[1 to 20 of 1 sentences]
75
[+] score: 3
Recent studies have demonstrated that miRNAs also play a role in obesity -induced cardiac pathophysiology 20, 21. miR-451 is involved in diabetic cardiomyopathy, such as cardiac hypertrophy through suppression of the LKB1/AMPK pathway in mice fed HFD [20]. [score:3]
[1 to 20 of 1 sentences]
76
[+] score: 3
Davidsen et al. (Davidsen et al. 2011) evaluated miRNAs that differed between high and low responders to a 12 week resistance training protocol and showed that expression of miRNAs 378, 29a, 26a was diminished in individuals who were low responders, but did not change in high responders, while expression of miR-451 increased only in low responders. [score:3]
[1 to 20 of 1 sentences]
77
[+] score: 3
The also revealed decreased expression of miR-148a and miR-451 in mouse PC, an observation consistent with other reports [40, 41, 55– 58]. [score:3]
[1 to 20 of 1 sentences]
78
[+] score: 3
No sign of hemolysis was detected in the samples as attested by dCq (miR-23a - miR-451) (Fig.   S7B), and the unchanged expression levels of let-7d-3p mmu-miR-21a-5p, two miRNAs that were not identified as colitis -associated, ruled out the possibility of a global circulating miRNA reduction due to anti-TNFα therapy (Fig.   S7C and D). [score:3]
[1 to 20 of 1 sentences]
79
[+] score: 3
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-17, hsa-mir-18a, hsa-mir-20a, hsa-mir-21, hsa-mir-22, hsa-mir-26a-1, hsa-mir-99a, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-106a, hsa-mir-107, mmu-let-7g, mmu-let-7i, mmu-mir-99a, mmu-mir-101a, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-126a, mmu-mir-127, mmu-mir-145a, mmu-mir-146a, mmu-mir-129-1, mmu-mir-206, hsa-mir-129-1, hsa-mir-148a, mmu-mir-122, mmu-mir-143, hsa-mir-139, hsa-mir-221, hsa-mir-222, hsa-mir-223, mmu-let-7d, mmu-mir-106a, hsa-let-7g, hsa-let-7i, hsa-mir-122, hsa-mir-125b-1, hsa-mir-143, hsa-mir-145, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-127, hsa-mir-129-2, hsa-mir-146a, hsa-mir-206, mmu-mir-148a, 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-18a, mmu-mir-20a, mmu-mir-21a, mmu-mir-22, mmu-mir-26a-1, mmu-mir-129-2, mmu-mir-103-1, mmu-mir-103-2, rno-let-7d, rno-mir-335, rno-mir-129-2, rno-mir-20a, mmu-mir-107, mmu-mir-17, mmu-mir-139, mmu-mir-223, mmu-mir-26a-2, mmu-mir-221, mmu-mir-222, mmu-mir-125b-1, hsa-mir-26a-2, hsa-mir-335, mmu-mir-335, 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-17-1, rno-mir-18a, rno-mir-21, rno-mir-22, rno-mir-26a, rno-mir-99a, rno-mir-101a, rno-mir-103-2, rno-mir-103-1, rno-mir-107, rno-mir-122, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-126a, rno-mir-127, rno-mir-129-1, rno-mir-139, rno-mir-143, rno-mir-145, rno-mir-146a, rno-mir-206, rno-mir-221, rno-mir-222, rno-mir-223, hsa-mir-196b, mmu-mir-196b, rno-mir-196b-1, hsa-mir-20b, hsa-mir-451a, mmu-mir-451a, rno-mir-451, hsa-mir-486-1, hsa-mir-499a, mmu-mir-486a, mmu-mir-20b, rno-mir-20b, rno-mir-499, mmu-mir-499, mmu-mir-708, hsa-mir-708, rno-mir-17-2, rno-mir-708, hsa-mir-103b-1, hsa-mir-103b-2, mmu-mir-486b, rno-mir-126b, hsa-mir-451b, hsa-mir-499b, mmu-mir-145b, mmu-mir-21b, mmu-let-7j, mmu-mir-130c, mmu-mir-21c, mmu-let-7k, hsa-mir-486-2, mmu-mir-129b, mmu-mir-126b, rno-let-7g, rno-mir-148a, rno-mir-196b-2, rno-mir-486
E [2] decreased miR-146a, miR 125a, miR-125b, let-7e, miR-126, miR-145, and miR-143 and increased miR-223, miR-451, miR-486, miR-148a, miR-18a, and miR-708 expression in mouse splenic lymphocytes [199]. [score:3]
[1 to 20 of 1 sentences]
80
[+] score: 3
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-mir-18a, hsa-mir-21, hsa-mir-23a, hsa-mir-26a-1, hsa-mir-30a, hsa-mir-99a, hsa-mir-103a-2, hsa-mir-103a-1, mmu-mir-1a-1, mmu-mir-23b, mmu-mir-30a, mmu-mir-99a, mmu-mir-126a, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-138-2, hsa-mir-192, mmu-mir-204, mmu-mir-122, hsa-mir-204, hsa-mir-1-2, hsa-mir-23b, hsa-mir-122, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-138-2, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-126, hsa-mir-138-1, mmu-mir-192, mmu-let-7a-1, mmu-let-7a-2, mmu-mir-18a, mmu-mir-21a, mmu-mir-23a, mmu-mir-26a-1, mmu-mir-103-1, mmu-mir-103-2, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-26a-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, hsa-mir-26a-2, hsa-mir-376c, hsa-mir-381, mmu-mir-381, mmu-mir-133a-2, rno-let-7a-1, rno-let-7a-2, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-18a, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-26a, rno-mir-30a, rno-mir-99a, rno-mir-103-2, rno-mir-103-1, rno-mir-122, rno-mir-126a, rno-mir-133a, rno-mir-138-2, rno-mir-138-1, rno-mir-192, rno-mir-204, mmu-mir-411, hsa-mir-451a, mmu-mir-451a, rno-mir-451, hsa-mir-193b, rno-mir-1, mmu-mir-376c, rno-mir-376c, rno-mir-381, hsa-mir-574, hsa-mir-652, hsa-mir-411, bta-mir-26a-2, bta-mir-103-1, bta-mir-16b, bta-mir-18a, bta-mir-21, bta-mir-99a, bta-mir-126, mmu-mir-652, bta-mir-138-2, bta-mir-192, bta-mir-23a, bta-mir-30a, bta-let-7a-1, bta-mir-122, bta-mir-23b, bta-let-7a-2, bta-let-7a-3, bta-mir-103-2, bta-mir-204, mmu-mir-193b, mmu-mir-574, rno-mir-411, rno-mir-652, mmu-mir-1b, hsa-mir-103b-1, hsa-mir-103b-2, bta-mir-1-2, bta-mir-1-1, bta-mir-133a-2, bta-mir-133a-1, bta-mir-138-1, bta-mir-193b, bta-mir-26a-1, bta-mir-381, bta-mir-411a, bta-mir-451, bta-mir-9-1, bta-mir-9-2, bta-mir-376c, bta-mir-1388, rno-mir-9b-3, rno-mir-9b-1, rno-mir-126b, rno-mir-9b-2, hsa-mir-451b, bta-mir-574, bta-mir-652, mmu-mir-21b, mmu-mir-21c, bta-mir-411b, bta-mir-411c, mmu-mir-126b, rno-mir-193b, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
Several miRNAs were found to be highly expressed in particular tissues: miR-204, -218, and -129-2-3p in brain tissues, miR-30a, -30e, -30d, -200a and -200b in kidney, miR-192 in liver, miR-451 in spleen, miR-21 in spleen and thymus, miR-193b, -378 in LDM muscle. [score:3]
[1 to 20 of 1 sentences]
81
[+] score: 3
Examples of such miRNAs include those that show enriched expression in brain tissue such as miR-451 and miR-488 (see [32]) and miRNAs that have been implicated in the etiology of other tumor types, such as miR-346 in follicular thyroid carcinoma [36]. [score:3]
[1 to 20 of 1 sentences]
82
[+] score: 3
As indicated in Table 2, among the top 20 miRNAs, miR-486, miR-16, miR-451 and miR-92a are mainly expressed by RBCs [9, 18] and account for 45% reads of the mapped miRNAs. [score:3]
[1 to 20 of 1 sentences]
83
[+] score: 2
For example, miR451 regulates a subset of pro-inflammatory cytokine to combat with influenza virus in mice DCs [14]. [score:2]
[1 to 20 of 1 sentences]
84
[+] score: 2
Other miRNAs from this paper: mmu-mir-451a
Khairul et al. [33] uncovered that under insufficient glucose metabolic stress, OCT1, activated by AMPK phosphorylation, negatively regulated miR451 to form a reciprocal feedback loop to assist glioblastoma multiforme cells to survive nutrient/energy starvation. [score:2]
[1 to 20 of 1 sentences]
85
[+] score: 2
We identified a second set of trans-eQTL on Chr 9 at ~107-108 Mb for miR-486 and miR-451, but the allele effects for these eQTL were not completely consistent (Additional file 1: Figure S6), thus we cannot conclude that these two trans-eQTL are one and the same. [score:1]
Allele Effects for miR-451 and miR-486 trans-eQTL on Chr 9. Figure S7. [score:1]
[1 to 20 of 2 sentences]
86
[+] score: 2
Kuwabara Y MicroRNA-451 exacerbates lipotoxicity in cardiac myocytes and high-fat diet -induced cardiac hypertrophy in mice through suppression of the LKB1/AMPK pathwayCirc Res. [score:2]
[1 to 20 of 1 sentences]
87
[+] score: 2
Of note, miR-451 was not sequenced from the NEBNext small RNA libraries. [score:1]
Of note, the levels of miR-122 and miR-451 in the vd2D media relative to the crude 2D media were reduced to a different extent, but not entirely abolished. [score:1]
[1 to 20 of 2 sentences]
88
[+] score: 2
To date, several dysregulated miRNAs have been demonstrated to be involved in NPC cell migration, invasion and metastasis, such as miR-29c, miR-451, miR-10b, miR-93, and miR-124 [17– 21]. [score:2]
[1 to 20 of 1 sentences]
89
[+] score: 2
Other miRNAs from this paper: mmu-mir-451a
Kuwabara Y, Horie T, Baba O, Watanabe S, Nishiga M, Usami S, et al. MicroRNA-451 exacerbates lipotoxicity in cardiac myocytes and high-fat diet -induced cardiac hypertrophy in mice through suppression of the LKB1/AMPK pathway. [score:2]
[1 to 20 of 1 sentences]
90
[+] score: 2
Specifically, we have detected out some regulators for lung non-specific genes, i. e., TF: ATF6, DBP (early), and TBP (late); miRNAs: mmu-mir-152, mmu-mir-187, mmu-mir-320, mmu-mir-326, mmu-mir-451 (early), and mmu-mir-494 (late). [score:2]
[1 to 20 of 1 sentences]
91
[+] score: 2
Defective erythroid differentiation in miR-451 mutant mice mediated by 14-3-3zeta. [score:1]
miR-451 protects against erythroid oxidant stress by repressing 14-3-3zeta. [score:1]
[1 to 20 of 2 sentences]
92
[+] score: 2
In various studies, several miRNAs, such as miR-451, miR-128, and miR-34, apparently regulate cancer stemness and drug resistance in breast cancer [7]. [score:2]
[1 to 20 of 1 sentences]
93
[+] score: 2
Samples with high levels of hemolysis observed visually or based on relative abundance of miRNA-451 (>23%), miRNA-16 (>13%) correlating with increase in miRNA-25, miRNA-106b, let-7 g and miRNA-93 were also excluded from analysis. [score:1]
miRNA-451 was found to be the most abundant in serum preparations, contributing to 22–23% of total miRNAs (Figure 2). [score:1]
[1 to 20 of 2 sentences]
94
[+] score: 2
Total RNA was extracted from the bead-bound exosomes and the expression of miR-1246, miR-451 and miR-122 were measured by qRT-PCR. [score:1]
miR-451 was not detectable in either the PDX mouse plasma or the NSG plasma. [score:1]
[1 to 20 of 2 sentences]
95
[+] score: 2
Unspecified Ambion and Exiqon company sequences, which are not as yet entered into the Sanger miR Database [37], were excluded from analysis but are listed in 1 and 2. Other miRs, such as miR-451 and miR-146a (from Ambion microarray data) or miR-21, miR-23 and miR-140 (from Exiqon microarray data) were also left out from further analysis because these miRs exhibited very low levels of expression in the retina compared with the mouse platform. [score:2]
[1 to 20 of 1 sentences]
96
[+] score: 1
Alternatively, hemolysis can more quantitatively be assessed by measuring the ratio of miR-451 (an erythrocyte-enriched miRNA) to miR-23a (a highly expressed and stable serum miRNA) abundance. [score:1]
[1 to 20 of 1 sentences]
97
[+] score: 1
Other miRNAs from this paper: mmu-mir-451a
These experiments suggest that miR-451 may decrease EMSY and CAB39, which could mediate the decrease in cell proliferation. [score:1]
[1 to 20 of 1 sentences]
98
[+] score: 1
With the exception for miR-451, Dicer deletion resulted in significant reduction of all of these miRNAs (Figure 1A, 10 weeks post tamoxifen). [score:1]
[1 to 20 of 1 sentences]
99
[+] score: 1
A recent study reported the Dicer1-independent biogenesis of miR-451, in which the catalytic activity of Argonaute2 was responsible for the pre-mir-451 hairpin cleavage process [65]. [score:1]
[1 to 20 of 1 sentences]
100
[+] score: 1
Redova M Poprach A Nekvindova J Iliev R Radova L Lakomy R Circulating miR-378 and miR-451 in serum are potential biomarkers for renal cell carcinomaJ Transl Med. [score:1]
[1 to 20 of 1 sentences]