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13 publications mentioning rno-mir-376b

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-376b. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 238
M [3]-mAChR inhibits H [2]O [2] induced upregulation of miR-376b-5p in H9c2 cellsTo examine further miR-376b-5p expression in ischemic myocardial cells and the effects of M [3]-mAChR on miR-376b-5p expression in vitro, H9c2 cells were co-incubated with H [2]O [2] (50 µM), choline (1 mM) or 4DAMP (5 nM) for 12 h. The results showed that H [2]O [2] significantly upregulated the miR-376b-5p expression (P<0.01) and this effect was antagonized by M [3]-mAChR agonist choline (Figure 3). [score:15]
To examine further miR-376b-5p expression in ischemic myocardial cells and the effects of M [3]-mAChR on miR-376b-5p expression in vitro, H9c2 cells were co-incubated with H [2]O [2] (50 µM), choline (1 mM) or 4DAMP (5 nM) for 12 h. The results showed that H [2]O [2] significantly upregulated the miR-376b-5p expression (P<0.01) and this effect was antagonized by M [3]-mAChR agonist choline (Figure 3). [score:10]
To confirm the expression changes of miR-376b-5p and miR-539 in myocardial ischemia, next we performed qRT-PCR analysis and found that miR-376b-5p and miR-539 were significantly upregulated upon myocardial ischemia and down-regulated by choline (P<0.05, Figure 1C and D). [score:9]
In the present study, for the first time, we found that miR-376b-5p inhibited the expression of BDNF and miR-376b-5p promoted H [2]O [2] -induced H9c2 cells injury, indicating that miR-376b-5p promoted myocardial ischemia injury possibly by inhibiting the expression of BDNF. [score:9]
Based on microarray analysis and further validation by qRT-PCR, we postulated that the upregulation of miR-376b-5p and miR-539 is involved in myocardial ischemia and M [3]-mAChR may protect against myocardial ischemia via the downregulation of miR-376b-5p and miR-539 expression. [score:9]
Our and luciferase assay experiments demonstrated that miR-376b-5p could directly bind to BDNF gene and inhibit its expression, providing support for our hypothesis that miR-376b-5p promotes myocardial ischemia injury possibly via the downregulation of BDNF. [score:8]
These data demonstrate that miR-376b-5p and miR-539 are significantly upregulated in ischemic heart of the rats and M [3]-mAChR agonist choline could reverse their upregulation. [score:7]
M [3]-mAChR inhibits the up-regulation of miR-376b-5p stimulated by H [2]O [2] in H9c2 cells. [score:6]
M [3]-mAChR inhibits H [2]O [2] induced upregulation of miR-376b-5p in H9c2 cells. [score:6]
To confirm that miR-376b-5p could directly bind to BDNF gene and inhibit its expression, a reporter construct with the insertion of a fragment of the 3′-UTR of BDNF mRNA containing the predicted miR-376b-5p binding site was transfected into HEK 293T cells. [score:6]
Taken together, these data prove that miR-376b-5p directly inhibits BDNF expression. [score:6]
These results are consistent with the results of gene array analysis verified by qRT-PCR (Figure 1C) and suggest that M [3]-mAChR inhibits the up-regulation of miR-376b-5p stimulated by H [2]O [2] in H9c2 cells. [score:6]
While miR-199a, miR-376b-5p, miR-539 and miR-106 were all significantly upregulated (more than 3 times compared to the control), only miR-376b-5p and miR-539 were downregulated to the level similar to the control group after treatment with choline. [score:6]
0032571.g003 Figure 3M [3]-mAChR inhibits the up-regulation of miR-376b-5p stimulated by H [2]O [2] in H9c2 cells. [score:6]
NF-κB mediates the inhibitory effect of M [3]-mAChR on miR-376b-5p expression in H9c2 cellsPrevious studies demonstrated that M [3]-mAChR could activate NF-κB [18]– [20]. [score:5]
Next we determined the expression of BDNF at the protein level in H9c2 cells and found that miR-376b-5p significantly reduced the expression of BDNF (P<0.05), and this reduction was reversed by AMO-376b-5p (Figure 4B). [score:5]
To further explore the role of miR-376b-5p in myocardial ischemia, we predicted the targets of miR-376b-5p by targetScan Release 5.1 online (www. [score:5]
TargetScan Release 5.1 was used to predict the target genes of miR-376b-5p. [score:5]
To determine the potential mechanism by which M [3]-mAChR inhibited miR-376b-5p expression, TFSEARCH was used to identify transcription factors that bind to the promoter of miR-376b-5p gene. [score:5]
Given recent studies demonstrating that BDNF was also expressed in the heart where it protected against myocardial ischemia injury [29]– [35], we proposed that BDNF is one potential target of miR-376b-5p in the heart. [score:5]
NF-κB mediates the inhibitory effect of M [3]-mAChR on miR-376b-5p expression. [score:5]
0032571.g005 Figure 5NF-κB mediates the inhibitory effect of M [3]-mAChR on miR-376b-5p expression. [score:5]
Collectively, these data strongly suggest that M [3]-mAChR inhibits miR-376b-5p expression via the activation of NF-κB. [score:5]
Therefore, we postulated that NF-κB possibly mediates the inhibitory effects of M [3]-mAChR on miR-376b-5p expression. [score:5]
NF-κB mediates the inhibitory effect of M [3]-mAChR on miR-376b-5p expression in H9c2 cells. [score:5]
Moreover, we found that M [3]-mAChR inhibited miR-376b-5p expression by activating NF-κB. [score:5]
Collectively, these data indicate that NF-κB mediates the inhibitory effect of M [3]-mAChR on miR-376b-5p expression. [score:5]
To our knowledge, this is the first report to demonstrate that miR-376b-5p promotes myocardial ischemia injury and that the cardioprotection of M [3]-mAChR against myocardial ischemia is at least partly mediated by the downregulation of miR-376b-5p. [score:4]
Rat miR-376b-5p, miR-539, 2′-O-methyl -modified antisense oligoribonucleotides of miR-376b-5p (AMO-376b-5p, miR-376b-5p inhibitor) and miR-376b-5p negative control (miR-NC) were synthesized by Shanghai GenePharma. [score:3]
H9c2 cells were pre -treated with H [2]O [2] (50 µM) for 12 h and then transfected with miR-376b-5p negative control (miR-NC), miR-376b-5p, miR-539, and 2′-O-methyl -modified antisense oligoribonucleotides of miR-376b-5p (AMO-376b-5p, miR-376b-5p inhibitor) for 24 h. (A). [score:3]
Furthermore, LPS significantly reduced miR-376b-5p expression (P<0.05, Figure 5D). [score:3]
showed that miR-376b-5p significantly enhanced H [2]O [2] -induced inhibition of H9c2 cells viability (P<0.05), which was reversed by AMO-376b-5p. [score:3]
These results suggest that BDNF is a target gene of miR-376b-5p. [score:3]
BDNF is a target gene of miR-376b-5p in cardiac myocytes. [score:3]
Although 1134 potential targets of miR-376b-5p were predicted, only a few of them have been reported to be involved in myocardial ischemia, including insulin-like growth factor 2 mRNA binding protein 2 [24], [25], ryanodine receptor 2 [26]– [28] and BDNF [29]– [35]. [score:3]
MiR-376b-5p level was upregulated more than 3 times after transfection (Figure S1), demonstrating the efficient transfection. [score:3]
BDNF level was determined by Western blot after H9c2 cells were transfected with miR-376b-5p negative control (miR-NC), miR-376b-5p and 2′-O-methyl -modified antisense oligoribonucleotides of miR-376b-5p (AMO-376b-5p, miR-376b-5p inhibitor) for 24 h. GAPDH served as loading control. [score:3]
Furthermore, LPS, NF-κB activator, significantly reduced miR-376b-5p expression. [score:3]
A fragment of the 3′-untranslated region (3′-UTR) of BDNF containing the putative miR-376b-5p binding sequence was cloned into psiCHECK-2 (Renilla luciferase vector) and the construct (0.5 µg) was transfected into HEK 293T cells with miR-NC, miR-376b-5p, AMO-376b-5p or AMO-376b-5p negative control (AMO-NC). [score:3]
MiR-376b-5p expression was determined by qRT-PCR. [score:2]
H9c2 cells were co-incubated with H [2]O [2] (50 µM), choline (1 mM) and 4DAMP (5 nM) for 12 h. MiR-376b-5p expression was determined by qRT-PCR. [score:2]
0032571.g004 Figure 4. (A) MiR-376b-5p binding site in 3′-untranslated region (3′-UTR) of BDNF gene. [score:2]
U6 as an internal control normalized miR-376b-5p for quantitative real-time (qRT-PCR). [score:1]
Next we measured miR-376b-5p expression by qRT-PCR in H9c2 cells treated with LPS (100 ng/ml), which is known to activate NF-κB in many previous studies [21]– [23]. [score:1]
H9c2 cells were transfected with miR-NC (100 nM), miR-376b-5p (100 nM), miR-539 (100 nM), miR-376b-5p (100 nM) and AMO-376b-5p (100 nM) using lipofectamine 2000 according to the manufacturer's instruction and incubated at 37°C for 24 h. Subsequently, cells were maintained in the culture until analysis [11]. [score:1]
To determine the involvement of miR-376b-5p and miR-539 in myocardial ischemia, we used H9c2 cells as an in vitro mo del. [score:1]
These results suggest that miR-539 is unlikely involved in myocardial ischemia and we focused on miR-376b-5p in the following experiments. [score:1]
Moreover, 3 binding sites of NF-κB were predicted on the promoter of miR-376b-5p gene by TFSEARCH (Figure 5A). [score:1]
The reporter construct was transfected into HEK 293T cells with miR-NC, miR-376b-5p, AMO-376b-5p or AMO-376b-5p negative control (AMO-NC). [score:1]
H [2]O [2]+miR-376b-5p. [score:1]
In conclusion, our results help establish that a novel M [3]-mAChR/NF-κB/miR-376b-5p/BDNF axis plays an important role in modulating cardioprotection. [score:1]
miR-376b-5p. [score:1]
MiR-376b-5p, not miR-539, reduced cell viability in H [2]O [2] -treated H9c2 cells. [score:1]
Moreover, miR-376b-5p significantly increased the intracellular ROS in H [2]O [2] -treated H9c2 cells (P<0.05) and this effect was reversed by AMO-376b-5p (Figure 2C). [score:1]
Therefore, we examined [Ca [2+]]i in H [2]O [2] -treated H9c2 cells and found that miR-376b-5p significantly increased the overload of [Ca [2+]]i (P<0.05) while AMO-376b-5p reversed this increase (Figure 2B). [score:1]
Taken together, these results suggest that miR-376b-5p promotes H [2]O [2] -induced H9c2 cells injury. [score:1]
MiR-376b-5p promotes H [2]O [2] induced H9c2 cells injuryTo determine the involvement of miR-376b-5p and miR-539 in myocardial ischemia, we used H9c2 cells as an in vitro mo del. [score:1]
Notably, miR-376b-5p but not miR-539 was implicated in reduced H9c2 cells viability induced by H [2]O [2]. [score:1]
qRT-PCR for miR-376b-5p, miR-539 was performed on a GeneAmp 5700 thermocycler using mirVanaTM miRNA Detection Kit following the manufacturer's instructions. [score:1]
H9c2 cells were transfected with miR-376b-5p for 24 h. MiR-376b-5p level was determined by quantitative real-time (qRT-PCR). [score:1]
Our results revealed for the first time that miR-376b-5p increased myocardial ischemia injury and was involved in M [3]-mAChR's cardioprotection. [score:1]
Furthermore, M [3]-mAChR antagonist 4DAMP reversed the effect of choline on miR-376b-5p. [score:1]
Therefore, miR-376b-5p and miR-539 appear to be involved in M [3]-mAChR mediated cardioprotection against myocardial ischemia. [score:1]
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2
[+] score: 37
Interestingly, the relative abundance of “A” to “I” editing of rno-miR-376 gradually increased during development and surpassed that of wild type isoform at P7, indicating that RNA editing may be a new strategy for the regulation of gene expression during brain development. [score:6]
Interestingly, results of this GO analysis are fully consistent with the high expression of the wild type rno-miR-376b and the edited isoform at early developmental stages and late postnatal stages, respectively. [score:4]
E. Developmental changes of the expression of wild type (WT) and “A” to “I” edited miRNA-376b at position 6 (A/G: 6). [score:4]
To further understand the biological significance of this editing event of rno-miR-376b, target prediction and GO analysis was introduced (Dataset S6). [score:3]
Predicted targets and GO annotation of wild type and edited rno-miR-376b (A/G: 6). [score:3]
Click here for file Predicted targets and GO annotation of wild type and edited rno-miR-376b (A/G: 6). [score:3]
We found that the predicted target genes of the wild type rno-miR-376 and the “A” to “I” edited isoform are of totally different functional groups (Figure 4F). [score:3]
Deep-sequencing results showed that the level of this “A” to “I” editing at position 6 of rno-miRNA-376b increased during cortical development. [score:2]
We found that the potential function of wild type rno-miR-376b may be mainly related to early developmental events including neuronal differentiation, cell migration, axon extension, and establishment or maintenance of neuronal polarity. [score:2]
F. Summary of biological processes that may be regulated by WT and edited (A/G:6) miRNA-376b. [score:2]
Sequenced PCR products were aligned to precursor sequence of miR-376b using the DNAstar program. [score:1]
As a distinguished representative of miRNA editing, rno-miRNA-376 family have been extensively studied [5]. [score:1]
For PCR verification of editing of miR-376b, genomic DNA and cDNA from P7 rat cortex were used as template. [score:1]
G. Validation of “A” to “I” editing of miRNA-376b at position 6. RNAs from P7 rat cortex were reverse transcribed and then amplified by PCR. [score:1]
The previously reported “A” to “I” editing at position 6 (A/G: 6) of rno-miRNA-376b was also detected in the present study by both deep-sequencing and PCR -based sequencing (Figure 4G). [score:1]
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3
[+] score: 27
Caspase-3 was a potential target of the downregulated miR-376b-3p, calpain 2 was a potential target of the upregulated miR-199a-3p, and iNOS was a potential target of downregulated miR-291a-5p (Figure  4B). [score:16]
The expression levels of miR-376b-3p and miR-137-3p were downregulated, but miR-144-3p was upregulated on the 14th day compared to the 3rd day after injury (Figure  3C). [score:8]
The increase in caspase 3 was consistent with its predicted miRNA, miR-376b-3p, which was downregulated on the 14th day compared to the 3rd day after avulsion. [score:3]
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4
[+] score: 13
Importantly, in the case of mir-376a-5p, mir-376b-5p, mir-376a-3p and mir-376-3p the edited nucleoside resides in the seed region, which is instrumental in targeting the miRNA to its target and could therefore lead to an altered target spectrum. [score:7]
In addition to known editing targets, such as mir-376b, we also identified the brain-specific mir-377 that was hitherto unknown to be edited. [score:3]
The most abundantly edited miRNA is mir-376b, in the brain (Figure 2B), fitting with the observation that in murine and human brains, mir-376a/b/c are targets of the RNA editing machinery [51, 52]. [score:3]
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5
[+] score: 7
The expression of one of these miRNAs (miR-376b-3p) through the life span is shown in Fig.   4. In males, the expression of miR-376b-3p at 2 weeks of age was >320-fold higher than the average expression at all other ages, while in females it was >150-fold higher. [score:7]
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6
[+] score: 7
There were several miRNAs involved in regulation of G-protein coupled receptors and differentially expressed in MMP-9 KO cardiomyocytes including down-regulated miR-376b as we have observed in I/R heart [34] and MMP-9 gene ablation leads to cardiomyocyte dysfunction. [score:7]
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7
[+] score: 7
The exeptions were miR-376a, which show a similar expression pattern as miR-376b-3p; and miR-23a, whose levels did not significantly rise from E20 to P2 (Table S1). [score:3]
INS-1E cells were used as a control for miRNA expression in beta-cells and all miRNAs could be detected in INS-1E cells except miR-376b-3p, -376a and -451. [score:3]
Interestingly, INS-1E cells contained precursor miRNA species for miR-451 and miR-376b-3p, but absence of mature miRNAs (Fig. S2). [score:1]
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8
[+] score: 5
Down-regulation of miR-23b contributes to activation of the TGF-b1/Smad3 signalling to terminate liver regeneration 33. miR-376b is involved in the IL6 signaling transduction system to prime liver regeneration 34. miRNAs can regulate lipid and bile acid metabolism which are involved in liver regeneration, thus the miRNAs may affect liver regeneration via lipid and bile acid. [score:5]
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9
[+] score: 4
Cultured DRG neurons transduced with lentiviral vectors expressing GFP, miR-21 or a control miRNA miR-376b. [score:3]
0023423.g004 Figure 4(a) to detect SPRY2 and PTEN protein in DRG neurons transduced with GFP, miR-21 or miR-376b (control) lentiviral vectors. [score:1]
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10
[+] 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-150, 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-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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11
[+] score: 3
Compared to the other 2 groups, 21 miRNAs are upregulated in 6-hour group as shown in the upper portion of Fig. 2, miR-9, miR-204, miR-335, miR-23a, miR-708, miR-146a, miR-325-5p, miR-106b, miR-143, miR-140, miR-376b-3p, miR-7a, miR-541, miR-185, miR-499, miR-127*, miR-320, miR-140*, miR-145*, miR-423*, miR-378. [score:3]
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12
[+] score: 2
Twelve miRNAs (miR-135a, miR-190, miR-22, miR-347, miR-376*, miR-380*, miR-382, miR-383, miR-702-3p, miR-708, miR-873, and miR-99b*) were regulated only in CCE rats (p < 0.05 vs. [score:2]
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13
[+] score: 2
A similar situation can be found in the human cluster {hsa-mir-368, HP-37, HN-7, hsa-mir-376a} which corresponds to the mouse {mmu-mir-376a, mmu-mir-376b, MP-38}. [score:1]
The fine-grained structure of these loci has some species-specific aspects, as illustrated by Figures 2 and 3. The figures show all the validated miRNAs in these regions, including those with suboptimal prediction scores from the Additional files 7, 8, and 9. We find that some miRNAs that are related in sequence, and have presumably arisen by duplication (such as the mir-368/mir-376-related sequences) have different numbers of copies in rodents and human. [score:1]
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