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34 publications mentioning rno-mir-150

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-150. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 132
Other miRNAs from this paper: hsa-mir-150
Interestingly, down-regulation of miR-150 by anti-miR-150 potentiated the increase of CXCR4 expression by Ado, and, on the opposite, up-regulation of miR-150 by pre-miR-150 prevented the increase of CXCR4 expression by Ado. [score:11]
In vitro, the mechanism involves A [2B] receptor activation, up-regulation of CXCR4 expression and down-regulation of miR-150. [score:9]
Transfection of cells with anti-miR-150 to inhibit miR-150 expression had no effect on CXCR4 expression or migration towards SDF-1α (Fig. 6D–E). [score:7]
Tano et al. [11] showed that ischemia inhibits the expression of miR-150 in bone marrow derived mononuclear cells and activates its target gene CXCR4. [score:7]
Increasing the expression of miR-150 by addition of pre-miR-150 did not affect CXCR4 expression, but blunted the increase of CXCR4 expression induced by Ado (Fig. 6F). [score:7]
Overall, it appears that up-regulation of CXCR4 expression by Ado may be controlled by multiple pathways involving both transcription of CXCR4 and of miR-150. [score:6]
These data suggest that, under ischemic conditions, Ado enhances CXCR4 expression through down-regulation of miR-150. [score:6]
Following ischemic stress, the expression of miR-150 in bone marrow derived mononuclear cells is inhibited [11]. [score:5]
Our results confirmed the expression of miR-150 in EPC and suggested that this miRNA may be a potential target to enhance the regenerative capacity of these cells. [score:5]
The mechanism involves A [2B] receptor activation, decreased expression of miR-150 and increased expression of CXCR4. [score:5]
Ado increased CXCR4 expression (A) and decreased miR-150 expression (B). [score:5]
Additional studies are required to test whether miR-150 affects the expression of other genes regulating the functionality of EPC. [score:4]
Knowing that CXCR4 is a target of miR-150 [11], this raises the possibility that miR-150 may be involved in the regulation of EPC recruitment to the ischemic heart. [score:4]
Blocking endogenous miR-150 with anti-miR-150 or enhancing the pool of intracellular miR-150 by transfection of pre-miR-150 did not alter CXCR4 expression per se. [score:3]
In parallel to an increase of CXCR4 expression, we observed a decrease of miR-150 when cells were treated with Ado. [score:3]
In HEK293T cells transfected with a reported plasmid containing the 3′ UTR of the CXCR4 gene, we observed an inhibition of luciferase activity upon administration of pre-miR-150 (Fig. 6C). [score:3]
Ultimately, the usefulness of miR-150 as a target for cardiac repair will have to be determined in animal mo dels. [score:3]
Cells were transfected with 20 nM HS_ADORA2B_6_HP (Qiagen, Venlo, The Netherlands), pre-miR [TM] miRNA precursor hsa-miR-150, anti-miR [TM] miRNA inhibitor hsa-miR-150 or their respective negative controls (Applied Biosystems, Lennik, Belgium). [score:3]
Since CXCR4 is a known target of miR-150 [11], we sought to verify this mechanism in our system. [score:3]
However, modulation of miR-150 expression by anti-miR-150 or pre-miR-150 did not affect cell migration. [score:3]
Interrogation of web-accessible databases identified over 400 predicted targets of miR-150. [score:3]
These results suggest that, in EPC subjected to ischemic conditions, the increase of CXCR4 expression by Ado is, at least in part, controlled by miR-150. [score:3]
Adenosine also increased CXCR4 under ischemic conditions, and decreased miR-150 expression. [score:3]
HEK-293T cells were plated into 96-well plates and co -transfected using Lipofectamine 2000 (Invitrogen) with 10 ng of a reporter plasmid containing the 3′ untranslated region (UTR) of CXCR4 inserted downstream of the Gaussian luciferase secreted reporter gene and the secreted alkaline phosphatase tracking gene (pEZX-MT05, GeneCopoeia, Labomics, Nivells, Belgium) and 30 nmol/L of pre-miR [TM] miRNA precursor hsa-miR-150 (Applied Biosystems) or negative control. [score:3]
Binding of miR-150 to the 3′ untranslated region of CXCR4 was verified by luciferase assay. [score:2]
Using a luciferase gene reporter assay, we were able to show that miR-150 indeed binds CXCR4 and thereby decreases CXCR4 expression. [score:2]
We therefore investigated whether Ado could regulate CXCR4 expression through modulation of miR-150. [score:2]
Associating anti-miR-150 with Ado significantly increased CXCR4 expression, compared to either treatment alone (Fig. 6D). [score:2]
So far, very few reports have studied miR-150 in stem cells. [score:1]
However, while miR-150 appears to slow EPC migration in our study, a previous study reported that miR-150, secreted by monocytes, enhances the migration of human microvascular endothelial cells [42]. [score:1]
Role of miR-150 in the effect of adenosine on CXCR4. [score:1]
C. HEK-293T cells were co -transfected with 10 ng of a reporter plasmid containing the 3′ UTR of CXCR4 and 30 nmol/L of either pre-miR control (control) or pre-miR-150 (miR-150). [score:1]
EPC were transfected with 30 nmol/L of anti-miR-150 or pre-miR-150, or respective controls, during 24 hours, and then treated with 10 µmol/L of adenosine during 6 hours in ischemic conditions. [score:1]
miRNA profiles have identified miR-150 in EPC, human umbilical vein endothelial cells, and human coronary artery endothelial cells [41]. [score:1]
Addition of pre-miR-150 blunted the effect of adenosine on CXCR4. [score:1]
This was paralleled by decreased miR-150 (Fig. 6B). [score:1]
However, anti-miR-150 did not enhance the effect of Ado on cell migration (Fig. 6E). [score:1]
CXCR4 and miR-150 expression was evaluated by PCR. [score:1]
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[+] score: 56
Correspondingly, in the high glucose media, expression of miR-144 was found to be highest (3.605±0.21) accompanied by a down-regulation of IRS1 (−3.257±0.29), followed by miR-150 (2.904±0.19) and miR-192 (1.989±0.20) which are predicted to target GLUT4 (−2.604±0.25) and CBL (−4.672±0.31) and INSR (1.150±0.28) respectively. [score:8]
Once again, the inverse pattern between miRNA and their mRNA target expression is demonstrated by both miR-150 and miR-320a up-regulation in T2D subjects (Fig. 5B, 6A). [score:8]
miR-29a, miR-144, miR-150, miR-192 and miR-320 showed an up-regulation from that of control samples whereas miR-30d, miR-146a and miR-182 showed down-regulation. [score:7]
miR-150, miR-182 and miR-30d showed contrasting expressions in IFG and T2D while miR-146a was down-regulated in both cases. [score:6]
CBL and GLUT4 are potential targets of miR-150, while miR-320 inhibits PI3-K/Akt signaling [50]. [score:5]
Among the novel miRNAs (miR-144, miR-146a, miR-150 and miR-182) identified, miR-144 had the highest up-regulation upon T2D in most tissues. [score:4]
In all five sources, miR-144, miR-150, miR-192, miR-29a and miR-320a were found to be highly up-regulated. [score:4]
Similarly, up-regulation of miR-150 was observed to be highest in the adipose (3.21±0.197) followed by liver (2.07±0.388). [score:4]
The eight miRNAs (miR-144, miR-146a, miR-150, mR-182, miR-192, miR-29a, miR-30d and miR-320) which were previously identified in the rat study showed similar expression in the patients' blood miRNAs. [score:3]
miR-29a, miR-30d, miR-150 and miR-320 are all highly expressed in adipose, skeletal muscle and liver tissues with lower abundance in pancreas. [score:3]
We have also identified eight important miRNAs (miR-144, miR-146a, miR-150, miR-182, miR-192, mir-29a, miR-30d and miR-320) that could participate in the regulation of insulin signaling as well as useful in distinguishing different stages of diabetes progression. [score:2]
Employing miRNA microarray and stem-loop real-time RT-PCR, we identify four novel miRNAs, miR-144, miR-146a, miR-150 and miR-182 in addition to four previously reported diabetes-related miRNAs, miR-192, miR-29a, miR-30d and miR-320a, as potential signature miRNAs that distinguished IFG and T2D. [score:1]
Predictions: miR-144/ IRS1; miR-146a/ PTPN1; miR-150/ GLUT4 and CBL; miR-182/ FOXO1; miR-192/ INSR; miR-30d/ INS; miR-29a and miR-320/ AKT2. [score:1]
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[+] score: 47
We found that the expression levels of other two miRNAs (i. e., miR-150 and miR-155) were up-regulated only in the vesicular-fraction, while the expression of both miR-21 and miR-33 was found to be up-regulated in RNA isolated from vesicles enriched pellets and down-regulated in the RNA isolated from vesicles -depleted sera. [score:14]
The expression of miRNA associated with infection and inflammation [i. e., miR-150 (P = 0.01) and miR-155 (P = 0.04)] is up-regulated through day 2 and 4, and declines at day 6 (Fig. 6, middle row). [score:6]
We now found that miR-150 is significantly up-regulated at both cellular and vesicular level in TWS-119 treated HSCs, suggesting that canonical Wnt signaling might be required to drive the expression of this miRNA. [score:6]
miR-150 was found to suppress HSCs activation 43, while Venugopal et al. have shown that expression of miRNA-150 was reduced in HSCs isolated from fibrotic livers 44. [score:5]
However, the expression of miRNAs associated to infection and inflammation (i. e., miR-150 and miR-155) is unchanged in the VDS fraction (Fig. 7, middle row), while the expression of regeneration -associated miRNAs [i. e., miR-21 (P = 0.01) and miR-33 (P = 0.02)] is significantly reduced in the VDS RNAs. [score:5]
On the other hand, miR-150 and miR-155 were found up-regulated only in the VEP fractions, while miR-21 and miR-33 were found differentially regulated across the two populations. [score:5]
A group of miRNAs whose expression is higher in the vesicle -depleted RNAs (i. e., miR-150, -30d, -122, -92a, -223 and -192, Fig. 5, left column). [score:3]
Among the regulated miRNAs, miR-150 is of great interest. [score:2]
Specifically, we found that the cytokines used in this study significantly increased levels of miR-122, miR-150, miR-21, miR-192 and miR-194 associated to EVs secreted from PCs. [score:1]
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[+] score: 37
Finally, through GO and pathway analysis of putative targets of individual miRNA, it was identified that certain miRNAs, including let-7f, regulated target genes associated with drug metabolism; certain miRNAs, including miR-150, regulated target genes associated with the response to glucose stimulation; numerous miRNAs, including miR-145, regulated genes associated with cell proliferation and apoptosis; and numerous other miRNAs, including miR-194, regulated genes associated with the inflammatory response. [score:11]
Stem-loop RT-PCR was used to confirm the expression levels of four selected miRNAs, in which miR-150 and miR-497 demonstrated upregulation, whereas miR-344-3p and let-7f showed downregulation, confirming the changes detected by the microarray (Fig. 1; P<0.05). [score:9]
By contrast, miR-150 was one of the upregulated miRNAs in GK rats and had 11 target genes downregulated in the GK rats (Fig. 3C). [score:9]
Among the miRNAs, miR-214, miR-199a-5p, miR-150, miR-199a-3p, miR-351, miR-145, miR-764, miR-497 and miR-92b were upregulated, whilst miR-7a, miR-325-5p, miR-485, miR-708, miR-344-3p, let-7f, miR-26b, miR-129, miR-29c and let-7a were downregulated. [score:7]
These miRNAs include miR-214, miR-199a-5p, miR-150, miR-351, miR-145, miR-92b, miR-7a, miR-485, miR-708, let-7f, miR-26b, miR-129, miR-29c and let-7a. [score:1]
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[+] score: 28
24-Hour Acute ZT06 Expression 24-Hour Chronic ZT06 Expression 2-Week chronic ZT06 Expression rno-miR-142-5p Over rno-miR-126a-5p Under rno-miR-146a-5p Under rno-miR-150-5p Over rno-miR-30b-5p Under rno-miR-24-3p Under rno-miR-335 Under rno-let-7b-5p Over rno-miR-130a-3p Over rno-miR-15b-5p Over rno-miR-99a-5p Over rno-miR-127-3p Under rno-miR-133a-3p Under rno-miR-10a-5p Over rno-miR-672-5p Over rno-miR-l-3p Under rno-let-7c-5p Over rno-miR-193-3p Over rno-miR-142-5p Under rno-miR-146b-5p Under rno-miR-150-5p Over Of the three ZT06 groups that illustrated differential expression of miRNAs due to CD, emphasis was placed on the two-week chronic ZT06 group due to the differential expression of miRs 146a and 146b, and miR-127 (Figures 5A-5B and 6A). [score:11]
24-Hour Acute ZT06 Expression 24-Hour Chronic ZT06 Expression 2-Week chronic ZT06 Expression rno-miR-142-5p Over rno-miR-126a-5p Under rno-miR-146a-5p Under rno-miR-150-5p Over rno-miR-30b-5p Under rno-miR-24-3p Under rno-miR-335 Under rno-let-7b-5p Over rno-miR-130a-3p Over rno-miR-15b-5p Over rno-miR-99a-5p Over rno-miR-127-3p Under rno-miR-133a-3p Under rno-miR-10a-5p Over rno-miR-672-5p Over rno-miR-l-3p Under rno-let-7c-5p Over rno-miR-193-3p Over rno-miR-142-5p Under rno-miR-146b-5p Under rno-miR-150-5p Over Differentially expressed miRNAs based on Illumina sequencing in all the circadian-disrupted samples and their links to breast cancer development and circadian rhythms. [score:10]
Between the ZT06 groups that showed differences in miRNAs, there were no significant correlations or patterns in specific miRNA expression, with only two miRNAs being differentially expressed in more than one group, miR-150-5p and miR-142-5p (Table 2). [score:5]
Although only two miRNAs were identified in more than one of the ZT06 groups, miR-142-5p and miR150-5p (Table 2), there are significant correlations and patterns related to breast cancer development in each ZT06 group. [score:2]
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[+] score: 19
DIV7 cultures were transfected with plasmids expressing empty vector, the control microRNA miR-150, or an Arc -targeting microRNA. [score:5]
After 7 days in vitro (DIV7), neurons were transfected with plasmids expressing DsRed only (empty vector), ds-Red-miR-150, DsRed-miR-326 or DsRed-miR-193a using Lipofectamine-2000 Reagent (Invitrogen). [score:3]
In panels A, B and C luciferase expression was normalized to the transfection control (gWIZ, alkaline phosphatase) and to miR-150. [score:3]
The luciferase values were further normalized to the average luciferase value obtained after transfecting a panel of microRNAs not predicted to target the rat Arc 3′UTR (rno-miR-370, rno-miR-150, rno-miR-342, rno-miR-30b, rno-miR-105, rno-miR-145 and rno-miR-9). [score:3]
Mean Arc levels were comparable between cells transfected with empty vector and miR-150 controls, but were significantly reduced in neurons transfected with miR-34a, miR-326, or miR-193a (Figure 4C and E). [score:1]
One day before transfection the medium was changed and replaced with fresh medium containing 2 mg/ml vitamin C. In the second set of experiments neurons were transfected with DsRed only, DsRed-miR150, or DsRed-miR34a using Lipofectamine LTX and Plus Reagent (Invitrogen) according to manufacturer's instructions. [score:1]
miR-150 was one of the miRNAs in the initial screen with least effect on the luciferase activity of the reporter vector. [score:1]
Cultured hippocampal neurons were transfected with either empty vector-DsRed, miR150-DsRed, miR34a-DsRed, miR326-DsRed or miR193a-DsRed. [score:1]
0041688.g004 Figure 4 Cultured hippocampal neurons were transfected with either empty vector-DsRed, miR150-DsRed, miR34a-DsRed, miR326-DsRed or miR193a-DsRed. [score:1]
[1 to 20 of 9 sentences]
[+] score: 18
MiR-150 was downregulated in the RV and, surprisingly, upregulated in plasma (Fig 1C and 1D). [score:6]
A group of miRNAs were downregulated in the lung and PA of MCT PAH rats, including miR-126, miR-145, miR-150, miR-424, and miR-503 (Fig 1A and 1B). [score:4]
An unexpected result was downregulation of miR-150 in MCT PAH tissue samples, but not plasma. [score:4]
N = 4. p values are as follows: MiR-126 p = 0.499, miR-145 p = 0.422, miR-150 p = 0.803. [score:1]
This result differed from findings in plasma of human PAH subjects which exhibited reduced plasma levels of miR-150 that correlated with poor survival [30]. [score:1]
Rather, miR-150 was significantly increased more than 1.5- fold (Figs 1D and 2) in plasma from MCT PAH rats. [score:1]
Expression levels of miR-17-5p, miR-21-5p, miR-126-3p, miR-145-5p, miR-150-5p, miR-204-5p, miR-223-3p, miR-328-3p, miR-424-5p (mmu-miR-322, the mouse/rat ortholog for hsa-miR-424), and miR-503-5p were evaluated. [score:1]
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[+] score: 17
Male-biased miRNA expression was associated with pathways related to cancer (miR-130b, miR-214, miR-181b, miR-199a, miR-150, miR-135a, miR-142-3p, miR-142-5p, miR-185), hematological disease (miR-22*, miR-142-3p, miR-142-5p, miR-150, miR-181b), and renal inflammation/nephritis (miR-130b, miR-223, miR-150, miR-142-5p, miR-296*, miR-185-3p) (Additional file 2). [score:5]
Three of these six molecules exhibited a pattern of increasing expression with age (miR-223, miR-150, miR-142-5p). [score:3]
Individual animal kidney fibrosis severity scores correlated positively and significantly (p < 0.05) with individual miR-142-5p (R = 0.526), miR-150 (R = 0.567), and miR-223 (R = 0.724) expression from those animals at 78 and 104 weeks of age. [score:3]
The expression of three miRNAs associated with fibrosis (miR-142-5p, miR-150, miR-223) was correlated with histopathology fibrosis severity scores. [score:3]
For example, miR-130b was found in pathways related to cancer, renal inflammation, and organismal injury and abnormalities, while miR-150 was found in both cancer and renal inflammation pathways. [score:1]
These six miRNAs are miR-130b, miR-296*, miR-223, miR-142-5p, miR-185, and miR-150. [score:1]
These miRNAs showed high representation in renal inflammation and nephritis pathways, and included miR-214, miR-130b, miR-150, miR-223, miR-142-5p, miR-185, and miR-296*. [score:1]
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[+] score: 15
miR-150 expression levels were not correlated with gender or EDSS. [score:3]
Multiple sclerosis Cerebrospinal fluid Biomarkers miRNA miR-219 miR-150 Multiple sclerosis (MS) is the most common chronic inflammatory demyelinating central nervous system (CNS) disease of young adults worldwide [1]. [score:3]
We found miR-150 to be significantly upregulated in relapse-onset (RRMS and SPMS) compared to PPMS patients. [score:3]
Pair-wise comparisons showed significant differences in mean levels of miRNA-150 between RRMS and PPMS (p = 0.007), and between progressive-onset (PPMS) and relapse-onset (RRMS + SPMS) disease (p = 0.023), but there were no differences compared to controls (Fig. 1f). [score:2]
e Percentage of CSF samples with undetected miR-219 in cohort 3. f Scatter plot of miR-150 relative expression levels in CSF of individuals with detectable miR-150 levels of cohort 3. miR-150 levels were significantly increased in RRMS compared to PPMS, and in relapse-onset (RRMS, SPMS) compared to progressive-onset (PPMS). [score:1]
However, after correction for age, only trends remained for the differences in the mean miR-150 levels between groups. [score:1]
No significant differences were found between miR-150 levels in relapse-onset patients who did or did not use interferon-beta. [score:1]
miR-150 was detectable in 55 of the 112 CSF samples, while the frequency of undetectable miR-150 was similar between groups in terms of insufficient RNA yield, insufficient total miRNA level, or insufficient miR-150 level. [score:1]
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[+] score: 12
Exemplification showed that miR-150 regulated cell proliferation by targeting VEGF [25], besides miR-382 negatively regulated PTEN expression and increased Akt phosphorylation during LR [35]. [score:7]
From the co -expression network, the obvious conclusion was that miR-150 was related with nine circRNAs, and miR-382 was related with 22 circRNAs. [score:3]
Likewise, in the network of the circRNA-miRNA co -expression at 6 h compared with CG, ten miRNAs binding with 71 circRNAs had closer connections among which miR-150-5p had been verified to play a vital part during rat LR (Fig.   3b) [24]. [score:2]
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[+] score: 11
Another miRNA, miR-150, was significantly up-regulated in LII at P09, and showed the same trend at P23 and P45, although up-regulation did not reach significance at these ages. [score:7]
Two miRNAs, miR-143 and miR-150, were up-regulated both in LII and in stellate neurons. [score:4]
[1 to 20 of 2 sentences]
[+] score: 9
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-17, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-32, hsa-mir-33a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-106a, mmu-let-7g, mmu-let-7i, mmu-mir-27b, mmu-mir-30a, mmu-mir-30b, mmu-mir-126a, mmu-mir-9-2, mmu-mir-135a-1, mmu-mir-137, mmu-mir-140, mmu-mir-150, mmu-mir-155, mmu-mir-24-1, mmu-mir-193a, mmu-mir-194-1, mmu-mir-204, mmu-mir-205, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-143, mmu-mir-30e, hsa-mir-34a, hsa-mir-204, hsa-mir-205, hsa-mir-222, mmu-let-7d, mmu-mir-106a, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-30b, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-137, hsa-mir-140, hsa-mir-143, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-126, hsa-mir-150, hsa-mir-193a, hsa-mir-194-1, mmu-mir-19b-2, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, 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-24-2, mmu-mir-29a, mmu-mir-31, mmu-mir-92a-2, mmu-mir-34a, rno-mir-322-1, mmu-mir-322, rno-let-7d, rno-mir-329, mmu-mir-329, rno-mir-140, rno-mir-350-1, mmu-mir-350, hsa-mir-200c, hsa-mir-155, mmu-mir-17, mmu-mir-25, mmu-mir-32, mmu-mir-200c, mmu-mir-33, mmu-mir-222, mmu-mir-135a-2, mmu-mir-19b-1, mmu-mir-92a-1, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-7b, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-106b, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-375, mmu-mir-375, 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-17-1, rno-mir-19b-1, rno-mir-19b-2, rno-mir-23a, rno-mir-24-1, rno-mir-24-2, rno-mir-25, rno-mir-27b, rno-mir-29a, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-31a, rno-mir-32, rno-mir-33, rno-mir-34a, rno-mir-92a-1, rno-mir-92a-2, rno-mir-106b, rno-mir-126a, rno-mir-135a, rno-mir-137, rno-mir-143, rno-mir-193a, rno-mir-194-1, rno-mir-194-2, rno-mir-200c, rno-mir-200a, rno-mir-204, rno-mir-205, rno-mir-222, hsa-mir-196b, mmu-mir-196b, rno-mir-196b-1, mmu-mir-410, hsa-mir-329-1, hsa-mir-329-2, mmu-mir-470, hsa-mir-410, hsa-mir-486-1, hsa-mir-499a, rno-mir-133b, mmu-mir-486a, hsa-mir-33b, rno-mir-499, mmu-mir-499, mmu-mir-467d, hsa-mir-891a, hsa-mir-892a, hsa-mir-890, hsa-mir-891b, hsa-mir-888, hsa-mir-892b, rno-mir-17-2, rno-mir-375, rno-mir-410, mmu-mir-486b, rno-mir-31b, rno-mir-9b-3, rno-mir-9b-1, rno-mir-126b, rno-mir-9b-2, hsa-mir-499b, mmu-let-7j, mmu-mir-30f, mmu-let-7k, hsa-mir-486-2, mmu-mir-126b, rno-mir-155, rno-let-7g, rno-mir-15a, rno-mir-196b-2, rno-mir-322-2, rno-mir-350-2, rno-mir-486, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
This spatial pattern of expression closely mirrors that of miR-23a, miR-143, and miR-150, all of which putatively target the Hoxa11 mRNA. [score:5]
Similarly, within the differentially expressed pool of miRNAs, 10 were identified that are intimately involved in regulating intracellular trafficking pathways, including: miR-7b-5p, miR-9-5p, miR-31-5p, miR-92a-3p, miR-106-5p, miR-126-3p, miR-150-5p, miR-204-5p, miR-222-3p, and miR-322-5p (S2 Fig). [score:4]
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[+] score: 9
Recent data have shown numerous miRNA dysregulations during MI, for example, MiR-210 and miR-1 were proven to improve cardiac function following MI by enhancing angiogenesis and inhibiting cardiomyocyte apoptosis [10, 11]; MiR-150 was shown to be downregulated in patients with acute myocardial infarction (AMI), atrial fibrillation, dilated cardiomyopathy and ischemic cardiomyopathy [12– 14]; and overexpression of microRNA-99a attenuates heart remo deling and improves cardiac performance following myocardial infarction [15]. [score:9]
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[+] score: 9
Eleven of the altered miRNAs were downregulated (miR-122, miR-93*, miR-872, miR-7*, miR-146a, miR-342-3p, miR-150, miR-139, miR-30a, miR-30e, miR-320), whereas three miRNAs, namely miR-463*, miR-34c* and miR-1188, were upregulated in the RYGB group. [score:7]
TCA cycle intermediates including citrate, succinate, 2-oxoglutarate and fumarate are positively correlated with miR-143, miR-126-3p, miR-146a, miR-150 and miR-155. [score:1]
In addition to miR-342-3p and miR-34c*, miR-872*, miR-463*, miR-30e, miR-2183, miR-1971, miR-150, miR-146a, miR-1188 and miR-93* all correlate with liver energy metabolism processes, such as glycolysis and glycogenesis involving glucose, glycogen and lactate. [score:1]
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[+] score: 9
Nine miRNAs (miR-21, miR-24, miR-214, miR-132, miR-195, miR-210, miR-144, miR-150 and miR-34a) were found in exosomes obtained from rats subjected to RIPC, but only miR-24 was significantly upregulated ([#] P < 0.05, n = 4). [score:4]
b, c Flow cytometric analysis of the uptake of exosomes by H9c2 cells at various time points We further determined the expression of nine miRNAs (miR-24, miR-21, miR-214, miR-132, miR-195, miR-210, miR-144, miR-150 and miR-34a) in both RIPC-EXO and EXO (Fig.   3a). [score:3]
Li X MicroRNA-150 aggravates H2O2 -induced cardiac myocyte injury by down -regulating c-myb geneActa Biochim. [score:1]
Since the subject of our study was IRI, we selected nine miRNAs that have been reported to be involved either in oxidative stress (such as miR-150 and miR-21) 14, 15 or in cardiomyocyte apoptosis (such as miR-195, miR-132, miR-140, miR-144, miR-24, miR-214 and miR-34a) 16– 21 in our investigation and, using quantitative PCR (qPCR), explored whether RIPC could modify the expression level of these nine miRNAs in plasma exosomes. [score:1]
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[+] score: 7
Four of these miRNAs were downregulated in the liver of rats born to DEX -treated mothers (miR-34a-5p, miR-34c-5p, miR-124-3-3p and miR-150-5p). [score:4]
Expression of miR-34a-5p, miR-34c-5p, miR-124-3p, and miR-150-5p (respectively, 52%, 56%, 47% and 20% lower than CTL; P < 0.05) but not miR-449a was reduced in the liver of 60-hour fasted rats born to DEX -treated mothers (Fig.   5G). [score:3]
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[+] score: 6
It was found to be a putative target for let-7 family members, miR-26ab, miR-181 family, miR-150, miR-27b, miR-23ab, miR-425, miR-125a-5p, and miR-128ab. [score:3]
Among the important genes were Lifr, Acvr1c, and Pparγ which were found to be targeted by microRNAs in our dataset like miR-143, miR-30, miR-140, miR-27b, miR-125a, miR-128ab, miR-342, miR-26ab, miR-181, miR-150, miR-23ab and miR-425. [score:3]
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[+] score: 5
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-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-mir-451b, 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
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]
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]
Dorsal root ganglion let-7c, miR-17, miR-145, miR-150, miR-199a, miR-223, miR-365, miR-451. [score:1]
Brain stem let-7c-1, miR-17, miR-135b, miR-150, miR-199a, miR-218-1, miR-223, miR-329. [score:1]
Hypothalamus miR-17, miR-29c, miR-124a-1, miR-128a, miR-150, miR-199a, miR-217, miR-223, miR-329, miR-429. [score:1]
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[+] score: 5
Particularly, it has been shown that some microRNAs (miRNAs) (e. g., miR-155, miR-146, miR-150) control the development and responses of the immune system [14]. [score:2]
Fig. 3Validation of miR130a-3p, miR-150-5p, miR-143-3p, and miR-223-3p in serum and lung tissues by qRT-PCR. [score:1]
Serum (c) and lung (d) levels of miR-150-5p in normal, IMD, and non-IMD rats. [score:1]
In contrast, there was no significant difference in the serum and lung levels of miR-150-5p, miR-143-3p, and miR-223-3p of among the normal, IMD, and non-IMD rats (P > 0.05, Fig.   3c–h). [score:1]
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[+] score: 4
Serum was collected from different stage at 1 [st] to 6 [th] week and the expression levels of 4 top ranked miRNAs (miR-25-3p, miR-140-5p, miR-342-5p and miR-150-5p) were assayed by qPCR. [score:2]
Conversely, miR-140-5p, miR-342-5p and miR-150-5p were not as stable as miR-25-3p and showed some notable changes at some stage (Fig. 2c). [score:1]
Therefore, ten miRNAs (miR-19b-3p, miR-21-5p, miR-25-3p, miR-30a-5p, miR-133b-3p, miR-140-5p, miR-150-5p, miR-199a-3p, miR-342-5p, miR-3473) were chosen as candidate reference genes. [score:1]
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[+] score: 4
We also tested miRNAs by RT-qPCR that were reported by others to change after radiation 13 and confirmed miR-150-5p was down regulated and miR-21-5p 18 was up regulated by radiation (Fig. 2b). [score:3]
Another two interesting miRNA (miR-150-5p and 21-5p) were selected for testing by RT-qPCR based on changes after radiation as reported by others. [score:1]
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[+] score: 3
For example, it has been reported that miR-221 [15], miR-199a/b [16][17], miR-27b [18], miR-195 [11] and miR-34a/b/c [19] positively regulate cardiac hypertrophy, while miR-378 [9], miR-29 [20], miR-150 [11], miR-223 [21] and miR-1 [22] negatively regulate cardiac hypertrophy. [score:3]
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[+] score: 3
For example, miR-150 is involved in heart disease via intercellular communication [36]. [score:3]
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[+] score: 3
An in vivo study of LPS administration to rats described amelioration of inflammation in response to a 20-hydroxyeicosatetraenoic acid analog in concert with decreases in miR-150 [40] In a recent review of miRNA in septic patients, changes in circulating levels of miR-150 and miR-146a were common findings, however any consistent association with clinical outcome remains ill-defined [27]. [score:1]
Among the individual miRNAs previously associated with endothelial cell and monocyte activation and sepsis in humans and rodents [27– 29], we found increases in our study of miR-16, miR-21, miR-126, miR-146a, miR-150, miR-511, and miR-23b. [score:1]
Among these, miR-150, miR-23b, and miR-146a have been previously identified as potential circulating mediators or biomarkers of inflammatory pathways in sepsis. [score:1]
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[+] score: 3
Most of the miRNAs in Fig.   4 were also highly expressed in the serum of normal adolescent rats, with the exception of mir-96, miR-96-5p, and miR-150-3p. [score:3]
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[+] score: 3
Other miRNAs from this paper: mmu-mir-30a, mmu-mir-101a, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-132, mmu-mir-134, mmu-mir-135a-1, mmu-mir-138-2, mmu-mir-142a, mmu-mir-150, mmu-mir-154, mmu-mir-182, mmu-mir-183, mmu-mir-24-1, mmu-mir-194-1, mmu-mir-200b, mmu-mir-122, mmu-mir-296, mmu-mir-21a, mmu-mir-27a, mmu-mir-92a-2, mmu-mir-96, rno-mir-322-1, mmu-mir-322, rno-mir-330, mmu-mir-330, rno-mir-339, mmu-mir-339, rno-mir-342, mmu-mir-342, rno-mir-135b, mmu-mir-135b, mmu-mir-19a, mmu-mir-100, mmu-mir-139, mmu-mir-212, mmu-mir-181a-1, mmu-mir-214, mmu-mir-224, mmu-mir-135a-2, mmu-mir-92a-1, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-125b-1, mmu-mir-194-2, mmu-mir-377, mmu-mir-383, mmu-mir-181b-2, rno-mir-19a, rno-mir-21, rno-mir-24-1, rno-mir-27a, rno-mir-30a, rno-mir-92a-1, rno-mir-92a-2, rno-mir-96, rno-mir-100, rno-mir-101a, rno-mir-122, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-132, rno-mir-134, rno-mir-135a, rno-mir-138-2, rno-mir-138-1, rno-mir-139, rno-mir-142, rno-mir-154, rno-mir-181b-1, rno-mir-181b-2, rno-mir-183, rno-mir-194-1, rno-mir-194-2, rno-mir-200b, rno-mir-212, rno-mir-181a-1, rno-mir-214, rno-mir-296, mmu-mir-376b, mmu-mir-370, mmu-mir-433, rno-mir-433, mmu-mir-466a, rno-mir-383, rno-mir-224, mmu-mir-483, rno-mir-483, rno-mir-370, rno-mir-377, mmu-mir-542, rno-mir-542-1, mmu-mir-494, mmu-mir-20b, mmu-mir-503, rno-mir-494, rno-mir-376b, rno-mir-20b, rno-mir-503-1, mmu-mir-1224, mmu-mir-551b, mmu-mir-672, mmu-mir-455, mmu-mir-490, 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-504, mmu-mir-466d, mmu-mir-872, mmu-mir-877, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-872, rno-mir-877, rno-mir-182, rno-mir-455, rno-mir-672, mmu-mir-466l, mmu-mir-466i, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-466j, rno-mir-551b, rno-mir-490, rno-mir-1224, rno-mir-504, mmu-mir-466m, mmu-mir-466o, mmu-mir-466c-2, mmu-mir-466b-4, mmu-mir-466b-5, mmu-mir-466b-6, mmu-mir-466b-7, mmu-mir-466p, mmu-mir-466n, mmu-mir-466b-8, rno-mir-466d, mmu-mir-466q, mmu-mir-21b, mmu-mir-21c, mmu-mir-142b, mmu-mir-466c-3, rno-mir-322-2, rno-mir-503-2, rno-mir-466b-3, rno-mir-466b-4, rno-mir-542-2, rno-mir-542-3
StAR may be a target gene of miR-376b, miR-150, miR-330 and miR-138. [score:3]
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[+] score: 3
Our previous human milk whey study also showed that miR-150 and miR-223 were present at higher levels in serum than in whey [6]. [score:1]
Comparison of whey and serum qPCR analyses using the same volumes of samples showed that only miR-192, miR-150, and miR-223 (apart from the tissue-specific miRNAs miR-451 and miR-122) were detected at higher levels in serum than in whey. [score:1]
Comparison of whey qPCR analyses using the same volumes of samples showed that levels of some miRNAs, such as let-7c, miR-29a, miR-29c, miR-192, miR-21, miR-146a, miR-150, miR-223, and miR-320, did not change during the lactation period (Fig. 6). [score:1]
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[+] score: 2
miR-125b, miR-146, miR-150, miR-199a, miR-21, miR-129, miR-341 and miR-451 have been confirmed to play an important role in the different developmental stages of the cardiovascular system (4– 18). [score:2]
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[+] score: 2
miR-210 and miR-150 protect the heart from ischemic injury by regulating cell death [16, 17]. [score:2]
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[+] score: 2
Lulla et al. identified that mir-135b, mir-150, mir-542-5p, and mir-652 were differentially expressed in osteosarcoma compared with normal osteoblasts [15]. [score:2]
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[+] score: 2
Furthermore, miR-194 and miR-150 regulated ECM synthesis and HSCs activation by reducing Ras-related C3 botulinum toxin substrate 1 and c-myb gene [13]. [score:2]
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[+] score: 1
In addition, our previous studies showed that miR-150 and miR-126 contributed to EPCs function in vitro and improved thrombus recanalization and resolution in vivo [14, 15]. [score:1]
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[+] score: 1
MicroRNA-150 protects the mouse heart from ischaemic injury by regulating cell death. [score:1]
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[+] score: 1
MiRNA from stressed, control, stress + prazosin, and control + prazosin rats were analyzed for changes in miR-142-5p, miR-150, miR-155, and miR-203. [score:1]
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