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11 publications mentioning rno-mir-151

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-151. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 136
Moreover, estrogen deficiency exacerbates acute MI -induced down-regulation of miR-151-5p, which may underlie the up-regulation of PLM protein level and down-regulation of Kir2.1 potassium channel expression. [score:12]
To explore the possible involvement of miRNAs in the expression regulation of PLM, we first measured the expression levels of miR-151-5p which have the potential to regulate its target gene (FXYD1) expression. [score:9]
Estrogen deficiency exacerbates MI -induced upregulation of PLM expression via down -regulating miR-151-5p. [score:7]
Our data also present the first demonstration that miR-151-5p can inhibits the expression of its target gene (FXYD1, Fig. 4a). [score:7]
Estrogen Deficiency Exacerbates MI -induced Upregulation of PLM Expression via Down -regulating miR-151-5p. [score:7]
miR-151-5p Represses PLM, Up-regulates Kir2.1 Expression and Decreases Intracellular Calcium Transient. [score:6]
Moreover, in all these cases, abnormal regulation of miR-151-5p is a common finding; therefore, keep balance of miR-151-5p expression may be a useful strategy for many diseases associated with miR-151-5p. [score:6]
As illustrated in Fig. 3A, miR-151-5p was significantly down-regulated in ventricular cardiac tissues of OVX +MI rats compared with MI animals, though OVX alone did not alter miR-151-5p expression. [score:5]
We first found that miR-151-5p was significantly down-regulated in ventricular cardiac tissues of OVX +MI rats compared with MI rats, though OVX alone did not alter miR-151-5p expression. [score:5]
HEK293 cells (1×10 [5]/well) were co -transfected with 1 µg PGL3–target DNA (firefly luciferase vector) and 20ng PRL-TK (TK -driven Renilla luciferase expression vector) with miR-151-5p mimics (NC, miR-151-5p+AMO-151-5p or AMO-151-5p, respectively) by lipofectamine™ 2000 according to the manufacturer’s instructions. [score:5]
These downstream alterations may be a mechanism underlying the ventricular arrhythmogenic potential of down-regulated miR-151-5p. [score:4]
We found that the duration of PVB prolonged after knockdown the expression of miR-151-5p with AMO-151-5p (Fig. S1A). [score:4]
Based on previous studies and the present data, it is speculated that miR-151-5p down-regulation may result in reduction of Kir2.1/I [K1], RP, Na [+]-K [+]-ATPase [38], [39] and Na [+]-Ca [2+] exchanger [34], [40], [41], leading to calcium and sodium overload in ventricular myocytes. [score:4]
These findings support the proposal that miR-151-5p could be a potential therapeutic target for the prevention of ischemic arrhythmias in post-menopausal women. [score:3]
An important finding in this study is that although estrogen deficiency alone does not alter cardiac electrophysiology and miR-151-5p expression, it indeed worsened the electrical disturbances in the setting of acute MI. [score:3]
rno-miR-151-5p (MIMAT0000613) (sense: 5′-UCGAGGAGCUCACAGUCUAGUAU-3′; antisense: 5′-ACUAGACUGUGAGCUCCUCGAAU-3′) and its antisense inhibitor AMO-151-5p were synthesized by GenePharma (Shanghai, China). [score:3]
The inhibitory effect of miR-151-5p was antagonized by its antisense AMO-151-5p. [score:3]
0072985.g003 Figure 3(A) Relative expression of miR-151-5p in rat hearts in each group. [score:3]
Effects of miR-151-5p on the expression of PLM (A) and Kir2.1 (B). [score:3]
Fig. 3B shown that miR-151-5p could bind to FXYD1 gene 3′-UTR based on computational prediction using the miRNA Microcosm Targets hosted by European Bioinformatics Institute [23], [24]. [score:3]
In conclusion, the increased ventricular arrhythmias vulnerability in response to acute ischemia in rats with estrogen deficiency is critically dependent upon down-regulation of miR-151-5p compared with MI heart only. [score:3]
In order to verify the effect of miR-151-5p knockdown on the increased ventricular arrhythmias vulnerability, we used in vivo gene transfer technique to transfect AMO-151-5p into myocardium. [score:2]
Figure S1 Effect of miR-151-5p knockout on the increased ventricular arrhythmias vulnerability in vivo. [score:2]
The ability of miR-151-5p to repress FXYD1 was verified by luciferase reporter activity assays in HEK293 cells that express minimal endogenous miR-151-5p (Fig. 3D). [score:2]
It should be noted that although our study identified miR-151-5p as an important factor in increasing susceptibility of MI -induced ventricular arrhythmias in rats with estrogen deficiency, it does not exclude other mechanisms for determining susceptibility of MI -induced ventricular arrhythmias, and our findings in experimental mo dels may not be applied directly to human ventricular arrhythmias. [score:2]
We observed here that miR-151-5p markedly decreased the resting [Ca [2+]] [i] in primary culture neonatal rat myocytes, and this decrease was abolished by AMO-151-5p (Fig. 5A, B). [score:1]
The present study revealed, for the first time, the role of miRNA in ischemic ventricular arrhythmias in rats with estrogen deficiency and miR-151-5p as a new arrhythmogenic miRNA acting on FXYD1. [score:1]
It is worth mentioning that miR-151-5p has been implicated in many other pathological conditions. [score:1]
Effects of miR-151-5p on the levels of intracellular calcium in neonatal cardiomyocytes. [score:1]
0072985.g004 Figure 4The totle protein samples were isolated from neonatal rat ventricular myocytes after 48 hours of transfection with miR-151-5p alone, miR-151-5p+AMO-151-5p, or a negative control (NC). [score:1]
For example, recent studies have shown that miR-151 is correlated with hepatocellular carcinoma cell migration and invasion [44]. [score:1]
We subsequently evaluated the ability of miR-151-5p to repress PLM and promote Kir2.1 expression in primary culture neonatal rat myocytes. [score:1]
Finally, the ability of the AMO-151-5p to cause calcium overload suggests the potential of miR-151-5p mimic as a drug for molecular conversion of ventricular arrhythmia to sinus rhythm. [score:1]
miR-151-5p repressed the resting intracellular calcium, which was effectively restricted by AMO-151-5p. [score:1]
Our study therefore suggests that a mechanism by which estrogen deficiency promotes ischemic arrhythmias may be mediated through the miR-151-5p–PLM–ion channel signaling pathway. [score:1]
As depicted in Fig. 4A, B, transfection of miR-151-5p remarkably reduced the protein level of PLM and increased the protein level of Kir2.1 and co-transfection of AMO-151-5p abolished the changes induced by miR-151-5p (Fig. 4A, B). [score:1]
Computational prediction has shown that miR-151-5p has potential to bind to FXYD1 gene 3′-UTR. [score:1]
The totle protein samples were isolated from neonatal rat ventricular myocytes after 48 hours of transfection with miR-151-5p alone, miR-151-5p+AMO-151-5p, or a negative control (NC). [score:1]
Primary cultured rat neonatal cardiamyocytes were transfected with miR-151-5p, AMO-151-5p, miR-151-5p+AMO-151-5p and NC using lipofectamine [TM]2000. [score:1]
miR-151-5p. [score:1]
Whether this low level of miR-151-5p participates in the increasing susceptibility of arrhythmia when estrogen is deprived? [score:1]
HEK293 cells were transfected with miR-151-5p alone, miR-151-5p+AMO-151-5p, AMO-151-5p alone or a negative control (NC) with lipofectamine 2000. [score:1]
miR-151-5p alone, unpaired Student’s t-test; n = 3 independent batches of cells for each group. [score:1]
These findings indicate the widespread pathophysiological function of miR-151-5p in humans. [score:1]
In our study, we found that the level of miR-151-5p decreased significantly in myocardial ischemia. [score:1]
Differences in expression of miR-151-5p between different RNA samples were calculated after normalization to U6. [score:1]
Normalization of miR-151-5p level to the normal range may well be a novel strategy for arrhythmic therapy in the clinical setting. [score:1]
Although miR-151-5p is involved in increasing susceptibility of MI -induced ventricular arrhythmias in rats with estrogen deficiency, whether it also plays a role in ventricular arrhythmia of other causes is unclear. [score:1]
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[+] score: 113
Using a consensus approach (i. e. a target must be predicted by at least four algorithms; see Methods and Materials for further detail), our bioinformatic analysis revealed that 356 putative mRNA targets of miR-23a-3p and 74 putative mRNA targets of miR-151-3p are expressed in hippocampal neuropil. [score:9]
MiR-23a and miR-151-3p are upregulated 5 h after LTP induction in vivoTo test our hypothesis that miRNAs are regulated in the MML neuropil that includes potentiated synapses 5 h after LTP induction, we carried out miRNA expression profiling of matched LTP-stimulated and control MML tissue using TLDAs (n = 4; Fig 2). [score:7]
It is also possible therefore, although unlikely, that the observed changes in miR-23a-3p and miR-151-3p expression contribute to plasticity via regulation of the minority synapses on the shafts of inhibitory interneurons or somata of these and other cell populations found in the MML. [score:6]
Neither was differentially expressed in the isolated granule cell layer, containing granule cell somata (miR-23a-3p: FC = 1.00 ± 0.15; p = 0.50; miR-151-3p: FC = 0.98 ± 0.13; p = 0.43; n = 7; Fig 5), although miR-132-3p was up-regulated (FC = 1.41; p = 0.03; data not shown) in keeping with previous research [13]. [score:6]
Through microarray expression profiling and RT-qPCR analysis we have identified two miRNAs in isolated neuropil, miR-23a-3p and miR-151-3p, which are up-regulated 5 h after LTP of perforant path-dentate gyrus synapses in vivo. [score:6]
We have demonstrated upregulation of miR-23a-3p and miR-151-3p in the MML 5 h after LTP induction in awake rats, thereby identifying two novel LTP-related miRNAs and demonstrating miRNA regulation in the neuropil in response to LTP induction in vivo for the first time. [score:5]
Upregulation of miR-23a-3p and miR-151-3p has not been reported in previous studies of miRNA regulation following LTP induction (Wibrand et al., 2010; Ryan et al., 2012b; Wibrand et al., 2012; Joilin et al., 2014; Pai et al., 2014; Park & Tang, 2009; Lee et al., 2012; Gu et al., 2015). [score:5]
Our observation that upregulation of miR-23a-3p and miR-151-3p is specific to the synaptodendritc compartment, and does not occur in the granule cell somatic layer, suggests that these miRNAs are regulated post-transcriptionally. [score:5]
Having found that miR-23a-3p and miR-151-3p were upregulated in the MML 5 h after LTP induction in vivo, we next explored the biological significance of this regulation. [score:5]
As both miR-23a-3p and miR-151-3p are known to be expressed in adult rat synapses [27], our findings suggest that these miRNAs may be involved in tight temporal control of protein expression at synapses in response to LTP induction. [score:5]
of the predicted synaptic targets of miR-151-3p indicated that they contribute to “Positive regulation of cellular component biogenesis” and “Cell projection organization”. [score:4]
While there was no correlation between LTP magnitude and miRNA fold change (data not shown), five miRNAs were upregulated: miR-132-3p (FC = 1.32 ± 0.08; p = 0.029); miR-7b-5p (FC = 1.38 ± 0.09; p = 0.025); miR-151-3p (FC = 1.16 ± 0.004; p < 0.001); miR-872-5p (FC = 1.48 ± 0.05; p = 0.011); and miR-23a-3p (FC = 1.73 ± 0.05; p = 0.005). [score:4]
Upregulation of miR-151-3p and miR-23a-3p was confirmed by single-plex RT-qPCR (dual criteria: one-tailed Student's t-test p < 0.05; fold change ± 0.15). [score:4]
MiR-23a and miR-151-3p are upregulated 5 h after LTP induction in vivo. [score:4]
The DAVID analysis of the predicted targets of miR-151-3p showed enrichment for the cluster of ontological terms including “Positive regulation of cellular component biogenesis” and “Cell projection organization” (enrichment score = 1.4). [score:4]
0170407.g004 Fig 4 Upregulation of miR-151-3p and miR-23a-3p was confirmed by single-plex RT-qPCR (dual criteria: one-tailed Student's t-test p < 0.05; fold change ± 0.15). [score:4]
Interestingly, a number of the predicted synaptic targets of miR-151-3p have been linked to intracellular trafficking: profilin 2 (PFN2) [38]; dynein, cytoplasmic 2, heavy chain 1 (DYNC2H1); Bardet-Biedl syndrome 4 (BBS4) [39]; and Bardet-Biedl syndrome 10 (BBS10). [score:3]
Validation of differential expression of miR-151-3p and miR-23a-3p in the dentate gyrus middle molecular layer 5 h after tetanisation. [score:3]
We also cannot discount the possibility that the observed changes in miR-23a-3p and miR-151-3p are occurring in glia resident in the neuropil; however, there is currently no evidence that either of these miRs is expressed in glia. [score:3]
Of the miRNAs identified in the discovery phase of our study, two were confirmed as differentially expressed in a second validation study in a separate group of animals (n = 7): miR-23a-3p (FC = 1.30 ± 0.10; p = 0.015) and miR-151-3p (FC = 1.17 ± 0.19; p = 0.045) (Fig 4). [score:3]
Having identified sets of putative neuropil-resident miR-23a-3p and miR-151-3p targets we probed the function of these mRNA sets using the functional annotation clustering tool in DAVID. [score:3]
MiR-151-3p and miR-23a-3p are not differentially expressed in the dentate gyrus granule cell layer 5 h after tetanisation. [score:3]
The magnitude of regulation for miR-151-3p was very similar to that of the TLDA result (FC = 1.17 versus 1.16), whereas regulation of miR-23a-3p was more modest (FC = 1.30 versus 1.73). [score:3]
Interestingly, regulation of both miR-151-3p and miR-23a-3p was specific to the MML. [score:2]
This suggests that miR-151-3p may regulate receptor/vesicle trafficking at the synapse in response to LTP induction. [score:2]
This suggests that miR-151-3p regulates synaptic reorganisation, which is associated with L-LTP [34, 35]. [score:2]
Predicted function of miR-23a-3p and miR-151-3p. [score:1]
Thus further work is required to explore the relationship between miR-23a-3p and miR-151-3p and LTP maintenance. [score:1]
As these studies did not quantify miRNAs specifically in the neuropil, it is likely that they were not able to detect such subtle changes in miR-23a-3p and miR-151-3p at the subcellular level. [score:1]
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[+] score: 9
The miRNA profile analysis showed that 38 miRNAs were differentially expressed between the HBC and CHB subjects; 33 were up-regulated, including miR-27a, miR-27b, miR-142-3p, miR-151-5p and miR-424, and 5 were down-regulated in HBC patients compared with the levels in CHB patients (fold-change>2.0 and P<0.01) (Table 2). [score:8]
For these experiments, 5 candidate miRNAs (miR-27a, miR-27b, miR-142-3p, miR-151-5p, and miR-424) were chosen because they were among in the 38 deregulated miRNAs in HBC compared with CHB. [score:1]
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[+] score: 9
In a recent study, downregulation of miR-151-3p was demonstrated during later stages of transverse aortic constriction -induced cardiac hypertrophy in mice, reflecting its participation in heart dysfunction [39]. [score:4]
The miR-151-3p level was decreased at late-stage diabetes in ZDF rats. [score:1]
Diminution in circulating levels was detected for miR-140, miR-151-3p, miR-185, miR-203, miR-434-3p and miR-450a (Figure 5). [score:1]
The miR-151-3p level were slightly increased at initial hyperinsulinemia and decreased at late-stage diabetes (Figure 5). [score:1]
At late-stage diabetes, the circulating level of 12 miRNAs was specifically altered; the circulating level of miR-375, miR-210 and miR-133a was increased, and the circulating levels of let-7i, miR-140, miR-450a, miR-185, miR-186, miR-151-3p, miR-203, miR-16 and miR-685 were strongly diminished versus their levels at the pre-diabetes stage (Figure 4). [score:1]
In our study, both the diminution of miR-151-3p and the strong increase in miR-133a level at late-stage diabetes could therefore be the consequence of heart muscle dysfunction. [score:1]
[1 to 20 of 6 sentences]
[+] score: 8
Moreover, significant changes in expression due to prenatal stress were found in miR-103 (down), miR-151 (down), and miR-219-2-3p (up). [score:3]
B, Table of putative target genes for modulated miRNAs (miR-103, miR-151, and miR-219-2-3p; p≤0.05) and their physiological functions. [score:3]
Non-stress groups), as observed by microarray analyses, the following candidates were selected for verification by qRT-PCR analysis: miR-151, miR-145, miR-425 (all down) and miR-103, miR-323, miR-98 (up) (Figure 3C). [score:1]
The following miRNAs were analyzed (5′ to 3′): mirR-181 and miR-186 (dams); miR-103, miR-151, miR-323, miR-145, miR-425, miR-98 (newborns). [score:1]
[1 to 20 of 4 sentences]
[+] score: 8
Further evidence pointed to miR-151’s protective effects being mediated via targeted suppression of c-Fos, a key regulator of apoptotic signaling [8]. [score:6]
MiR-151 knockout mice have recently been used to demonstrate miR-151’s protection against cisplatin -induced kidney injury [7]. [score:2]
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[+] score: 7
Dentate gyrus lysates were immunoprecipitated with an Ago2-specific antibody or control, non-immune IgG, and expression of the brain-specific miRNAs, miR-151, and miR-347, was examined by qPCR. [score:3]
The quality of the total RNA was assessed by PCR-Quality Control (PCR-QC) using TaqMan® Gene expression assays (Applied Biosystems, Life Sciences, Carlsbad, CA, USA) for amplification of miRNAs which are known to express in the brain: miR-347 (assay 1334) and miR-151 (assay 1330). [score:2]
TaqMan qPCR for brain-enriched miR-347 and miR-151 was performed in Ago2 immunoprecipitated (IP) or non-immune mouse IgG immunoprecipitated samples from dentate gyrus. [score:1]
miR-151 and miR-347 levels were enriched more than 100-fold in the Ago2 IP (Figure 1A). [score:1]
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[+] score: 4
However miR-151*, miR-10a-5p, miR-205, miR-17-5p, miR-145 and miR-664 were up-regulated in the AcarH group (fold change>2, P<0.05, Table 2, Figure 4). [score:4]
[1 to 20 of 1 sentences]
[+] score: 3
Eleven miRNAs, including miR-145-5p, miR-34c-5p, miR-365-3p, miR-214-3p, miR-151, miR-27a, miR-153-5p, miR-365-3p, miR-33-5p, miR-217-5p and miR-129-5p, were differentially and significantly expressed (P < 0.05; Figure 2B). [score:3]
[1 to 20 of 1 sentences]
[+] score: 1
Reference miRNAs (rno-miR-27b-3p, rno-miR-21-5p, rno-miR-151-3p, rno-miR-191a-5p, mmu-miR-351-5p, rno-miR-125a-5p, rno-miR-181a-5p) were selected using geNorm [6], and reached stability criteria. [score:1]
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[+] score: 1
Additionally all reads of sequences originally reported in miRbase as the minor strand (*) were grouped (upon similar criteria as above; Table S5) resulting in a further 58 miRNAs of interest, 16 of which (including miR-126*, miR-140*, miR-151* and miR-28*) were detected between 1.23 and 99.56 fold higher in the * form than the ‘major’ mature sequence, while miR-501* was not detected in the major mature strand form. [score:1]
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