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39 publications mentioning rno-mir-208b

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-208b. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 230
We found that down-regulation of miR-208b-3p decreased the percentage of H9c2 cells in the early phase of apoptosis and inhibited expression of cleaved caspase-3 and Bax, while it increased Bcl-2 expression. [score:10]
Since one miR can regulate the expression of its target gene through both transcription and post-transcription mechanisms, we inferred that miR-208b-3p incompletely complementary binds to the 3’-UTR of Ets1, which only inhibits translation after transcription and prevents synthesis of the protein, while not impacting the stability of the mRNA. [score:10]
We can conclude that LUT attenuates apoptosis after I/R injury through down-regulation of miR-208b-3p and up-regulation of Ets1 expression. [score:9]
C. Transfecting Nc mimic/inhibitor had no statistical significance on the expression of cleaved caspase-3, Bax and Bcl-2. A. MiR-208b-3p was detected to be up-regulated under A/R injury, LUT pretreatment could down-regulate it in H9c2 cells, ** p<0.01, * p<0.05 as compared with control group; ## p<0.01 as compared with AR group. [score:8]
Transfection with the miR-208b-3p mimic significantly increasedmiR-208b-3p expression levels by 296.10 ± 27.63-fold versus the Nc mimic group (p < 0.001) (Fig 5A), and transfection with the miR-208b-3p inhibitor decreased the level of miR-208b-3p in cultured H9c2 cells by 0.14 ± 0.04-fold versus the Nc inhibitor group (p < 0.05) (Fig 5B). [score:7]
It is significant in such a process that down-regulation of miR-208b-3p results in an increase in Ets1 expression. [score:6]
Among the four down-regulated miRs, changes in miR-146b-5p and miR-208b-3p expression levels were obvious. [score:6]
A major finding of this study was that miR-208b-3p expression significantly reduced Ets1 protein levels, but had no significant effect on mRNA levels, suggesting that miR-208b-3p regulates Ets1 expression at the post-transcription level. [score:6]
Briefly, H9c2 cells were co -transfected with the WT/MUT GP-Check2 vector containing Ets1 3’-UTR and miR-208b-3p mimic/inhibitor using Lipofectamine 2000, while co-transfection with a non -targeting RNA sequence served as a negative control. [score:5]
Overexpression of miR-208b-3p caused a significant decrease in luciferase activity (p < 0.001), and transfection with the miR-208b-3p inhibitor increased luciferase activity (p < 0.01), suggesting that. [score:5]
Knockdown of miR-208b-3p expression also attenuated apoptosis, while knockdown of Ets1 promoted apoptosis. [score:5]
Our present results showed that miR-208b-3p expression levels were up-regulated in H9c2 cells, as compared to the control group. [score:5]
B. Transfecting miR-208b-3p inhibitor (208i group) could significantly knock-down miR-208b-3p expression in H9c2 cells, *** p<0.001 as compared with Ni group. [score:5]
Ets1 was predicted as one of the putative target genes of miR-208b-3p by TargetScan (www. [score:5]
The relative expression levels of miR-208b-3p and its target gene, Ets1, were detected by the standard curve method, and normalized against U6 and β-actin, respectively. [score:5]
LUT pretreatment could down-regulate miR-208b-3p expression, *** p<0.001 as compared with IR group. [score:5]
After overexpression and knockdown miR-208b-3p, A/R and LUT pre-treatment, AV/PI dyeing was used to determine the percentage of H9c2 cells in the early phase of apoptosis by flow cytometry. [score:4]
MiR-208b-3p was detected to be up-regulated under A/R injury, LUT pretreatment could down-regulate it in H9c2 cells, ** p<0.01, * p<0.05 as compared with control group; ## p<0.01 as compared with AR group. [score:4]
To examine whether miR-208b-3p regulates the expression of Ets1, a dual luciferase GP-Check2 reporter plasmid (Shanghai GenePharma Co. [score:4]
However, the mechanisms regarding how LUT regulates the expression of miR-208b-3p remain unclear. [score:4]
LUT pre-treatment down-regulates miR-208b-3p during A/R. [score:4]
This result provides a possible basis of miR-208b-3p regulation of Ets1 expression and an ultimate effect on cellular activities. [score:4]
, Shanghai, China), of which the sense sequence was the same as that of miR-208b-3p or complementary to miR-208b-3p, to overexpress or knockdown miR-208b-3p. [score:4]
Further, the luciferase reporter assay showed that miR-208b-3p could inhibit Ets1 expression. [score:4]
Also, overexpression or knockdown of miR-208b-3p had no significant effect on Ets1 mRNA levels (p > 0.05 vs. [score:4]
Thus, we concluded that overexpression of miR-208b-3p aggravates apoptosis and knockdown of miR-208b-3p alleviates apoptosis. [score:4]
We also found that miR-208b-3p overexpression abolished the protect effects of LUT. [score:3]
In addition, the roles of miR-208 in heart diseases, such as myocardial hypertrophy [37] and myocardial fibrosis [38], have also been reported. [score:3]
Transfection with the miR-208b-3p mimic decreased Ets1 protein levels, while transfection with the miR-208b-3p inhibitor increased Ets1 protein levels (p < 0.05, 208m+AR and 208i+AR groups vs. [score:3]
The RT-qPCR results showed that, as compared to the control group, A/R injury increased miR-208b-3p expression (4.37 ± 0.12, p < 0.01), while LUT pre-treatment reduced miR-208b-3p expression in the H9c2 cells, as compared to the AR group (2.23 ± 0.43, p < 0.01) (Fig 7A). [score:3]
H9c2 cells were plated in a 6-well plate at a concentration of 3×10 [5] cells per well and transfected with a specific miR-208b-3p mimic or a duplex RNA inhibitor (Shanghai GenePharma Co. [score:3]
However, overexpression of miR-208b-3p further aggravated the changes caused by I/R and blocked all the effects of LUT. [score:3]
Ets1 is a target gene of miR-208b-3p. [score:3]
LUT pretreatment conveys anti-apoptotic effects after myocardial I/R injury by decreasing miR-208b-3p and increasing Ets1 expression levels. [score:3]
C. Knocking down miR-208b-3p expression under AR decreased the early apoptotic cell percentage of H9c2 cells compared with Ni+AR group (* p<0.05). [score:3]
Cells were transfected by miR-208b-3p mimic, inhibitor and small interfering RNA of Ets1 (avian erythroblastosis virus E26 (v ets) oncogene homolog 1). [score:3]
Ets1 mRNA was detected to have no statistical significance under miR-208b-3p mimic/inhibitor transfecting (p>0.05). [score:3]
LUT was found to reduce miR-208b-3p expression, thereby attenuating apoptosis. [score:3]
Ets1 was a target of miR-208b-3p. [score:3]
The literatures of miR-208 on cardiovascular diseases were more than miR-146. [score:3]
On the other hand, transfection with the miR-208b-3p inhibitor was found to decrease the percentage of H9c2 cells in the early phase of apoptosis (21.47 ± 2.33% vs. [score:3]
After LUT pre-treatment and transfection with the miR-208b-3p mimic/inhibitor, Ets1-siRNA was found to affect the percentage of H9c2 cells in the early phase of apoptosis. [score:3]
And LUT decreased miR-208b-3p expression and apoptosis caused by I/R. [score:3]
B. RT-qPCR detected miR-208b-3p expression in perfusion myocardial tissue. [score:3]
To better elucidate the mechanism between miR-208 and myocardial I/R injury, we performed the experiments described in this report according to some of the methods reported by Fang et al. [17], who used a miR microarray to analyze an in vivo rat mo del of 4-h myocardial ischemia without reperfusion and found that miR-378 overexpression conveyed a protective role to cardiomyocytes following ischemic injury. [score:3]
A. RT-qPCR verified the overexpression of miR-208b-3p by transfecting miR-208b-3p mimic (208m group) in H9c2 cells, *** p<0.001 as compared with Nm group. [score:2]
B. Overexpression of miR-208b-3p under AR significantly increased the early apoptotic cell percentage of H9c2 cells compared with AR group (***p<0.001). [score:2]
LUT pretreatment reduced miR-208b-3p expression in myocardial tissue, as compared to the I/R group. [score:2]
We inferred that LUT might also reduce the production of miR-208b-3p or induce miR-208b-3p degradation through epigenetic modification, signal pathway or regulating specific transcription factors. [score:2]
C. By transfecting of the reporter plasmid with (WT group) or without (MUT group) the putative miR-208b-3p binding site, the luciferase activity decreased after miR-208b-3p overexpression and increased after miR-208b-3p knock-down in H9c2 cells; *** p<0.001 as compared with WT+Nm group, ** p<0.01 as compared with WT+Ni group. [score:2]
Accordingly, the anti-apoptotic effect of LUT is dependent on knockdown of miR-208b-3p. [score:2]
A luciferase reporter assay was used to verify the combination between miR-208b-3p and the 3’-untranslated region of Ets1. [score:2]
The results of showed that LUT pre-treatment reduced miR-208b-3p expression in the myocardiocytes, as compared to I/R group (0.37 ± 0.04, p < 0.001) (Fig 2B). [score:2]
RT-qPCR verified the overexpression of miR-208b-3p by transfecting miR-208b-3p mimic (208m group) in H9c2 cells, *** p<0.001 as compared with Nm group. [score:2]
Knocking down miR-208b-3p decreased cleaved caspase-3 and Bax, ### p<0.001, ## p<0.01 as compared with AR group. [score:1]
Knocking down miR-208b-3p increased Bcl-2, # p<0.05 as compared with AR group. [score:1]
In recent years, studies of miR-208 mainly concentrated on plasma biomarkers [33], acute myocardial infarction [34], heart failure [35], and ventricular remo deling [36]. [score:1]
However, there have no reports on the relationship between miR-208 and apoptosis of myocardiocytes following I/R injury. [score:1]
However, LUT pre-treatment had no effect on the A/R -induced changes following transfection with the miR-208b-3p mimic (p > 0.05) (Fig 4B). [score:1]
In addition, mutating the predicted binding site of miR-208b-3p (MUT+208m, MUT+208i group) abolished the process mentioned above (p>0.05). [score:1]
In addition, of the predicted miR-208b-3p binding site abolished this process (p > 0.05) (Fig 7C). [score:1]
Knocking down miR-208b-3p increased Ets1, # p<0.05 as compared with AR group. [score:1]
AV/PI dual staining revealed that after transfection with the miR-208b-3p mimic, the percentage of H9c2 cells in the early phase of apoptosis increased (54.60 ± 2.05% vs. [score:1]
The complicated mechanism between miR-208 and myocardial I/R injury needs to be further explored. [score:1]
Studies have reported that miR-208 is specific to myocardiocytes, at least to some extent [32, 33]. [score:1]
The results of a large-scale clinical trial demonstrated that miR-208 could be detected in the blood of patients after early acute myocardial infarction [33]. [score:1]
Therefore, we cloned the 3’-UTR of Ets1 downstream of a luciferase gene and mutated the predicted binding site of miR-208b-3p in the 3’UTR of Ets1 as a mutative plasmid. [score:1]
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[+] score: 58
Figure S5 Conservation of (A) Timp3 miR-1/206 targeting seed, (B) Rbm24 miR-125b-5p targeting seed, (C) Tgfbr2 miR-204 targeting seed, (D) Csnk2a2 miR-208b targeting seed. [score:9]
It is noteworthy that miR-1, miR-133, miR-30, miR-208a, miR-208b, mir-499, miR-23a, miR-9 and miR-199a have previously been shown to be functionally involved in cardiovascular diseases such as heart failure and hypertrophy [40], [41], [42], [43], [44], and have been proposed as therapeutic- or disease-related drug targets [45], [46]. [score:7]
Although the 3 myomiRs miR-208a/miR-208b/miR-499 contain almost identical seed sequences, miR-499 was considerably less potent at inhibiting luc-Csnk2a2 expression than miR-208a/miR-208b, suggesting a functional role for 3′ compensatory interactions between the myomiRs and Csnk2a2 (Figure 7D and H). [score:5]
A subset of microRNAs (miR-1, miR-125b-5p, miR-204 and miR-208b) was selected for further cross-species analysis and their expression level relative to heart apex is shown in Figure 4. MiR-1 was highly expressed in all rat, dog and cynomolgus monkey heart structures except valves. [score:5]
In particular, several microRNAs that are preferentially expressed in different types of muscles (e. g. miR-1, miR-133, and the myomiRs miR-208, miR-208b and miR-499) play a pivotal role in maintenance of cardiac function [17], [18], and the ablation of microRNAs-RISC machinery can have dramatic effects on cardiac development [19], [20], [21]. [score:4]
We selected 4 genes (Timp3, Rbm24, Tgfbr2 and Csnk2a2), respectively targeted by miR-1, miR-125b, miR-204 and miR-208b, for further analysis. [score:3]
MiR-208b over -expression led to a 25% decrease in Csnk2a2 mRNA levels in HPASM cells (Figure 7D), and a 50% inhibition of luciferase activity in HEK cell reporter assays (Figure 7H). [score:3]
In contrast, expression profiles of miR-204/Tgfbr2 in canine and cynomolgus monkey, as well as miR-208b/Csnk2a2, in cynomolgus monkey were positively correlated. [score:3]
Casein kinase 2a2 (Csnk2a2) and miR-208ab have both previously been implicated in cardiovascular pathologies [29], [40], [54] and our data provide further support for cardiac tissue miR208-Csnk2a2 interactions based on their anti-correlated (<−0,8) expression profiles. [score:3]
In summary, we have demonstrated that four genes (Timp3, Rbm24, Tgfbr2 and Csnk2a2) important for cardiac/muscular physiology are post-transcriptionally regulated by miR-1, miR-125b-5p, miR-204 and miR-208b and exhibit conserved cardiac tissue miR-mRNA interactions across species. [score:2]
We have also identified novel microRNA -mediated post-transcriptional mRNA regulatory interactions with potentially important roles in cardiac/muscle physiopathology including miR-1/Timp3, miR-125b/Rbm24, miR-204/Tgfbr2 and miR-208b/Csnk2a2. [score:2]
MiR-208b expression was high in myocardium structures but very low in the atria of rat and dog and in valves of all the three species. [score:2]
Attempts to stain miR-208b via ISH were unsuccessful. [score:1]
Distribution of miR-1, miR-125b-5p, miR-204 and miR-208b in cardiac structures across species. [score:1]
Here we focused on the characterization of four microRNAs, including myocardial specific miR-1 and miR-208b and valve enriched mir-204 and miR-125b-5p, based on their distinct heart-structure-specific distribution patterns and known roles in cardiac physiology, disease and pathological remo deling. [score:1]
An assessment of the degree of conservation for structure-specific distribution of microRNAs in Wistar rat, Beagle dog and cynomolgus monkey (see for relative enrichment analysis), revealed high enrichment of nine microRNAs cardiac valves (miR-let7c, mIR-125b, miR-127, mir-199a-3p, miR204, miR-320, miR-99b, miR-328 and miR-744) (Figure 3A) and seven microRNAs in the myocardium (miR-1, mir-133a, miR-133b, miR-208b, miR-30e, miR-499-5p, miR-30e*) (Figure 3A). [score:1]
0052442.g006 Figure 6 Timp3 and miR-1 (A), Rbm24 and miR-125b-5p (B), Tgfbr2 and miR-204 (C), Csnk2a2 and miR-208b (D). [score:1]
0052442.g007 Figure 7 (A–D) Real-Time RT-PCR of Timp3, Rbm24, Tgfbr2 and Csnk2a2 in HPASM cells transfected with mimics for miR-1, miR-125b-5p, miR-204, miR-499 and miR-208b or with a mimic microRNA negative control. [score:1]
Conserved microRNA signatures were identified in valves (miR-let-7c, miR-125b, miR-127, miR-199a-3p, miR-204, miR-320, miR-99b, miR-328 and miR-744) and in ventricular-specific regions of the myocardium (miR-1, miR-133b, miR-133a, miR-208b, miR-30e, miR-499-5p, miR-30e*) of Wistar rat, Beagle dog and cynomolgus monkey. [score:1]
Timp3 and miR-1 (A), Rbm24 and miR-125b-5p (B), Tgfbr2 and miR-204 (C), Csnk2a2 and miR-208b (D). [score:1]
Furthermore, ventricular microRNAs (miR-1, miR-133, miR-208b and miR-499) have been found to be increased in the plasma of patients with myocardial infarction, and might represent a useful alternative to the classical cardiac troponin (cTnI) biomarker [57], [58], [59], [60], [61]. [score:1]
Figure S6 Distribution of miR-1, miR-125b-5p, miR-204 and miR-208b in the cardiac structures in 1 human donor. [score:1]
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[+] score: 35
Consistent with previous work, the DOX -induced expression of miR-208b parallels the modulation of expression of its host gene Myh7 (Figure S1B) and occurs in parallel to the appearance of vacuolation (Table S3). [score:5]
Comparable changes for many of these microRNAs were confirmed in additional animals, and a subset of five microRNAs (miR-208b, miR-215, miR-216b, miR-367 and miR-34c) and were largely unaffected by the direct Top2 inhibitor etoposide (EPS) (Figure 3). [score:4]
Following two weeks treatment with DOX alone, a slight up-regulation of miR-208b, mir-216b and miR-367 was observed in the heart of most animals. [score:4]
Treatment with DOX at all doses and time points was associated with sustained up-regulation of these microRNAs, together with miR-208b and miR-215 at later time points. [score:4]
Five of these microRNAs (miR-208b, miR-215, miR-216b, miR-34c and miR-367) displayed a consistent dose -dependent response to DOX at 2 and 4 weeks and were thus chosen as candidates for further expression profiling across the larger in vivo study treatment groups including co-treatment of DOX with DZR and treatment with EPS only (Figure 3). [score:3]
MiR-367, miR-215, miR-216b, miR-208b and miR-34c are Specifically Dysregulated by Chronic DOX Treatment. [score:2]
0040395.g003 Figure 3Relative quantification of (A) miR-208b, (B) miR-215, (C) miR-216b, (D) miR-367 and (E) miR-34c in DOX, DOX + DZR, EPS groups, normalized versus vehicle treated animals. [score:1]
In summary, chronic treatment with DOX at 3 mg/kg/week for 2 weeks led to increases in miR-208b, miR-216b and miR-367, with fold change intensities comparable to those shown by genomic cardiomyopathy indicators (Ankrd/Carp, Nppb, Myh7 and Myh6) (Figure 2 and Table 1), suggesting that microRNAs may enhance the predictivity of established genomic indicators of drug -induced cardiomyopathy (e. g. myosin genes, troponins, natriuretic peptides) when assessing the potential for drug -induced cardiotoxicity. [score:1]
Therefore miR-208b may be implicated in the pathology mechanism of the vacuolation. [score:1]
Following 6 weeks of treatment with DOX alone, the levels of miR-208b, miR-215, miR-216b and miR-367 were significantly increased. [score:1]
Increasing doses of DOX led to higher cumulative vacuolation grading with time (S1 and Table S2), as well as progressively larger fold changes for microRNAs miR-208b, miR-216b and miR-367 versus vehicle. [score:1]
Following 4 weeks of treatment with DOX alone, the level of all five microRNA candidates were significantly increased and dose dependency was observed for miR-208b, miR-215, miR-216b and miR-367. [score:1]
Interestingly, we observed that miR-208b profile across treatment groups had the best statistically significant correlation score in comparison to the severity of vacuolation (Spearman R squared  = 0.76, p = 4.45E-04) (S1 and Table S3). [score:1]
Relative quantification of (A) miR-208b, (B) miR-215, (C) miR-216b, (D) miR-367 and (E) miR-34c in DOX, DOX + DZR, EPS groups, normalized versus vehicle treated animals. [score:1]
After treatment with the combination of DOX at 2 mg/kg/week and DZR at 50 mg/kg/week, the level of miR-208b, miR-216b and miR-367 was either slightly increased or not affected. [score:1]
Following 6 weeks of treatment with the same DOX/DZR combination, the level of miR-208b, miR-216b and miR-367 was increased. [score:1]
Treatment with DOX in H9c2 did not affect the level of miR-208b ruling out a potential implication of miR-208b with autophagy in this cellular mo del. [score:1]
MicroRNA-208b, encoded from the intron 28 of rat Myh7, is associated to maintenance of myocardial performance together with 2 other myomirs, i. e. miR-208a/miR-499, which play a pivotal role in the myosin balance [40]. [score:1]
Immunochemistry staining of autophagy markers like Ambra1 in heart tissues will also be required to elucidate the functional involvement of miR-215, miR-216b, miR-367, miR-208b and miR-34c in the DOX -induced autophagy process since they seem to be specifically associated to vacuoles appearance. [score:1]
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[+] score: 25
Of these, miR-208b-3p and miR-133b-were significantly up-regulated in HF and returned towards normal levels in HF-R (Fig.   5A). [score:4]
Hsa-/mmu-miR-1a-3p, identical to rno-miR-1b, and hsa-/mmu-miR-208b-3p, was also highly expressed in the sheep LV. [score:3]
Our data indicate that hsa-/mmu-miR-208b-3p (previously miR-208b) was the main miR-208 isoform expressed in the sheep heart. [score:3]
Two isoforms of miRNA-208-a/b have also been reported in humans, with miRNA-208a exclusively expressed in the heart and miRNA-208b found in both cardiac and skeletal muscle [34]. [score:3]
For the first time we report that not only are the four cardiac-enriched miR-1, miR-133, miR-499 and miR-208 highly expressed in sheep LV, but also provide information on their isomiRs. [score:3]
Four myocardial-enriched miRNAs, miR-1, miR-133, miR-499 and miR-208, were confirmed to be highly expressed in ovine heart tissue. [score:3]
Validation of a selected few by qPCR identified 10 miRNAs - miR-133b-3p, miR-208b-3p, miR-21-5p, miR-125a-5p, miR-125b-5p, miR-126-3p, miR-210-3p, miR-29a-3p, miR-494-3p and miR-320a, that were significantly up-regulated in HF myocardium compared to normal controls. [score:3]
Hsa-/mmu-/rno-miR-208b-3p was the most abundant form of the miR-208 family. [score:1]
MiR-1, miR-133, miR-499 and miR-208 are highly enriched myocardial miRNAs 27, 28 and are highly conserved across multiple species including human [29], mouse [30] rat [31] and porcine [32]. [score:1]
Cardiac-enriched miR-1-3p, miR-133a-3p, miR-133b-3p, miR-208b-3p and miR-499-3p were screened. [score:1]
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[+] score: 25
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-20a, hsa-mir-22, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-98, hsa-mir-101-1, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-15b, mmu-mir-101a, mmu-mir-126a, mmu-mir-130a, mmu-mir-133a-1, mmu-mir-142a, mmu-mir-181a-2, mmu-mir-194-1, hsa-mir-208a, hsa-mir-30c-2, mmu-mir-122, mmu-mir-143, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-181a-1, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-15b, hsa-mir-122, hsa-mir-130a, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-142, hsa-mir-143, hsa-mir-126, hsa-mir-194-1, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-208a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-18a, mmu-mir-20a, mmu-mir-22, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-29c, mmu-mir-98, mmu-mir-326, rno-mir-326, rno-let-7d, rno-mir-20a, rno-mir-101b, mmu-mir-101b, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-181b-2, mmu-mir-17, mmu-mir-19a, mmu-mir-181a-1, mmu-mir-26a-2, mmu-mir-19b-1, mmu-mir-181b-1, mmu-mir-181c, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-101-2, hsa-mir-26a-2, hsa-mir-378a, mmu-mir-378a, hsa-mir-326, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-181b-2, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-15b, rno-mir-16, rno-mir-17-1, rno-mir-18a, rno-mir-19b-1, rno-mir-19a, rno-mir-22, rno-mir-26a, rno-mir-26b, rno-mir-29c-1, rno-mir-30c-1, rno-mir-30c-2, rno-mir-98, rno-mir-101a, rno-mir-122, rno-mir-126a, rno-mir-130a, rno-mir-133a, rno-mir-142, rno-mir-143, rno-mir-181c, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-194-1, rno-mir-194-2, rno-mir-208a, rno-mir-181a-1, hsa-mir-423, hsa-mir-18b, hsa-mir-20b, hsa-mir-451a, mmu-mir-451a, rno-mir-451, ssc-mir-122, ssc-mir-15b, ssc-mir-181b-2, ssc-mir-19a, ssc-mir-20a, ssc-mir-26a, ssc-mir-326, ssc-mir-181c, ssc-let-7c, ssc-let-7f-1, ssc-let-7i, ssc-mir-18a, ssc-mir-29c, ssc-mir-30c-2, hsa-mir-484, hsa-mir-181d, hsa-mir-499a, rno-mir-1, rno-mir-133b, mmu-mir-484, mmu-mir-20b, rno-mir-20b, rno-mir-378a, rno-mir-499, hsa-mir-378d-2, mmu-mir-423, mmu-mir-499, mmu-mir-181d, mmu-mir-18b, mmu-mir-208b, hsa-mir-208b, rno-mir-17-2, rno-mir-181d, rno-mir-423, rno-mir-484, mmu-mir-1b, ssc-mir-15a, ssc-mir-16-2, ssc-mir-16-1, ssc-mir-17, ssc-mir-130a, ssc-mir-101-1, ssc-mir-101-2, ssc-mir-133a-1, ssc-mir-1, ssc-mir-181a-1, ssc-let-7a-1, ssc-let-7e, ssc-let-7g, ssc-mir-378-1, ssc-mir-133b, ssc-mir-499, ssc-mir-143, ssc-mir-423, ssc-mir-181a-2, ssc-mir-181b-1, ssc-mir-181d, ssc-mir-98, ssc-mir-208b, ssc-mir-142, ssc-mir-19b-1, hsa-mir-378b, ssc-mir-22, rno-mir-126b, rno-mir-133c, hsa-mir-378c, ssc-mir-194b, ssc-mir-133a-2, ssc-mir-484, ssc-mir-30c-1, ssc-mir-126, ssc-mir-378-2, ssc-mir-451, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, mmu-mir-378b, mmu-mir-101c, hsa-mir-451b, hsa-mir-499b, ssc-let-7a-2, ssc-mir-18b, hsa-mir-378j, rno-mir-378b, mmu-mir-133c, mmu-let-7j, mmu-mir-378c, mmu-mir-378d, mmu-mir-451b, ssc-let-7d, ssc-let-7f-2, ssc-mir-20b-1, ssc-mir-20b-2, ssc-mir-194a, mmu-let-7k, mmu-mir-126b, mmu-mir-142b, rno-let-7g, rno-mir-15a, ssc-mir-378b, rno-mir-29c-2, rno-mir-1b, ssc-mir-26b
Expression analysis of conserved miRNAs in 14 different tissue types revealed heart-specific expression of miR-499 and miR-208 and liver-specific expression of miR-122. [score:7]
Consistently, miR-208 is specifically and abundantly expressed in the heart, but we found a very weak expression (trace levels) in lungs (Figure 2A). [score:5]
Some miRNAs, including miR-208, miR-101, miR-18a, miR-20 and miR-142-3p, showed a weaker expression than other miRNAs tested by small RNA blot analyses (Figures 2 and 3). [score:3]
These results are in agreement with the expression analysis of miR-208 in rats and humans [48]. [score:3]
Because of their location within the introns of myosin genes and their specific expression in myogenic cells, miR-208 and miR-499 were referred to as MyomiRs [47]. [score:3]
Several miRNAs (miR-1, miR-133, miR-499, miR-208, miR-122, miR-194, miR-18, miR-142-3p, miR-101 and miR-143) have distinct tissue-specific expression patterns. [score:3]
miR-208 is encoded in intron 27 of the human and mouse αMHC gene [48]. [score:1]
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[+] score: 20
Our results showed that GS-Rb1 could suppress the expression of mir-208 in mo del group. [score:5]
But there was no enough evidence shown that overexpression or knockdown mir-208 was related to the hypoxia/ischemia injuries and cardiomyocytes apoptosis. [score:4]
MicroRNAs have been proved to be potential biomarkers for ischemic heart disease, such as mir-1, mir-133, mir-208, and mir-499 [4– 6]. [score:3]
The expression level of mir-1, mir-29a, and mir-208 was increased in the H/I group (5.9-, 3.4-, and 9.3-fold versus control, relatively), while that of mir-21 and mir-320 was significantly decreased (0.35- and 0.41-fold versus control, relatively). [score:3]
Compared with that of the control group, expressions of mir-1, mir-29a, and mir-208 obviously increased in the experimental mo del groups. [score:2]
Plasma mir-208 increased significantly after isoproterenol -induced myocardial injury and showed a similar time course to the concentration of cTnI [35]. [score:1]
A growing number of studies have demonstrated that mir-208 could be selected as a possible biomarker of myocardial injury and myocardial infarction [33, 34]. [score:1]
The relationship of mir-208 and cardiomyocytes injury or cell apoptosis needs to be further studied. [score:1]
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[+] score: 19
MiR-16 inhibited apoptosis of ESCC cells by downregulating RECK and SOX6 [9]; miR-208 [8] and miR-155 [11] promoted ESCC or hepatocellular carcinoma cell proliferation by targeting SOX6. [score:8]
MiR-499 and miR-21 were downregulated in LPS -induced cells in a dose- and time -dependent manner, while there was no significant change to miR-1, miR-133, and miR-208 expression. [score:6]
In the myocardium of rats with acute myocardial infarction, the expression of some miRNAs was altered, including cardiac-abundant miRNAs such as miR-1, miR-133, miR-208, and miR-499 [15– 17]. [score:3]
Cardiac-abundant miRNAs such as miR-1, miR-133, miR-208, and miR-499 regulate diverse aspects of cardiac function, including cardiomyocyte proliferation, differentiation, contractility, and stress responsiveness. [score:2]
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[+] score: 17
Examples of the expression profiles of miRNAs that change with age and/or sex are shown in Figures  5 and 6. Female-biased miRNA expression is illustrated by miR-421*, miR-499, and miR-208* (Figure  5A-C), all of which showed female-biased expression at 15 and 21 weeks. [score:7]
MiR-208* showed the highest fold change difference between sexes with female expression approximately 16 and 21-fold higher than male expression at 15 and 21 weeks of age, respectively. [score:4]
Those DEMs exhibiting female bias (17 miRNAs, Additional file 3) included miRNAs showing the highest fold-change differences between sexes (miR-208*, with 21-fold change F > M) and most prolonged, sex-biased expression (miR-421*, at 15, 21, 78, and 104 weeks). [score:3]
The miRNA showing the greatest fold-change difference between the sexes was miR-208* which showed approximately 21-fold higher expression in females compared to males at 21 weeks of age (Table  2 and Figure  5). [score:2]
Female-biased miRNAs feature some of the most promising candidates (miR-421*, miR-499, miR-208*) to further investigate the potential impact of sex-biased expression of miRNAs in the kidney. [score:1]
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[+] score: 15
Among them, 12 miRNAs (rno-miR-10b-5p, rno-miR-122-5p, rno-miR-184, rno-miR-1843-5p, rno-miR-196c-5p, rno-miR-199a-5p, rno-miR-202-5p, rno-miR-206-3p, rno-miR-208b-5p, rno-miR-224-5p, rno-miR-298-5p and rno-miR-31a-5p) were significantly upregulated(p<0.01, fold-change >1) compared to the control group and only rno-miR-208a-3p were significantly downregulated (p<0.01, fold-change <-1) (Fig 3). [score:6]
We found that in the heart failure group, miR-208b were up regulated, while the miR-208a-3p expression increased in the early stage after myocardial infarction, but decreased in the late stage, indicating that miR-208a-3p and miR-208b play different even opposite roles in heart failure, which needs to be clarified by further research. [score:4]
MiR-208 family members are highly expressed in cardiomyocytes, and are closely related with ventricular remo deling [34]. [score:2]
The miR-208 family includes two subfamilies: miR-208a and miR-208b. [score:1]
In the first miRNA deletion animal mo del in 2007, miR-208, a cardiac-specific miRNA, was found to be required for cardiomyocyte hypertrophy and fibrosis[8]. [score:1]
Whether or not miR-208 contributes to fibrosis is not fully elucidated. [score:1]
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[+] score: 14
The direct target of miR-208 has been shown to be p21 [25], and p21 expression in vascular smooth muscle cells has been shown to be crucial in limiting vascular proliferation in vascular remo deling, which is strongly associated with essential hypertension [26]. [score:6]
We found that miR-208 is upregulated in insulin -mediated proliferation of vascular smooth muscle cells and may promote a switch from the G0/G1 phase of the cell cycle to the S phase. [score:4]
In our studies, the most frequently observed and the most promising miRNAs as potential treatment targets are miR-145 [11] and miR-208 [25]. [score:3]
The miRNAs miR-1, miR-155, and miR-208 have significant effects on the RAAS [14]. [score:1]
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[+] score: 14
To be specifically mentioned (fold change >2.5), miR-208, miR-19b, miR-133b and miR-30e were significantly upregulated and miR-99b, miR-100, miR-191a, miR-22 andmiR-181a-1 were significantly downregulated. [score:7]
miR-208b THRAP1, Myostatin The expression of miR-208b was upregulated during physiological cardiac hypertrophy. [score:6]
We found that miR-99, miR-100, miR-208, miR-181, miR-19 and many others were associated to cardiac hypertrophy and apoptosis. [score:1]
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[+] score: 14
Other miRNAs from this paper: rno-mir-208a
Mir-208 is expressed specifically in the heart with trace expression in the lung [9]. [score:4]
The constructed plasmid (co -expression mir-208 and green fluorescent protein) was transfected into left ventricular myocardium using a low pressure-accelerated gene gun (Bioware Technologies, Taipei, Taiwan) essentially following the protocol from the manufacturer. [score:3]
The 165 bp amplified product was digested with EcoRI and BamHI restriction enzymes and ligated into pmR-ZsGreen1 plasmid vector (coexpression mir-208 and green fluorescent protein, Clontech Laboratories, Mountain View, CA, USA) digested with the same enzymes. [score:3]
Mir-208 expression vector was transfected into left ventricular myocardium by low pressure-accelerated gene gun. [score:2]
In brief, each 15 µl RT reaction contained purified 10 ng of total RNA, 3 µl miR-208 RT primer (Applied Biosystems®, Life Technologies, Grand Island, NY, USA), 1×RT buffer (Applied Biosystems), 0.25 mM each of dNTPs, 3.33 U/µl MultiScribe™ reverse transcriptase (Applied Biosystems) and 0.25 U/µl RNase inhibitor (Applied Biosystems). [score:2]
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[+] score: 14
Three miRNAs profiles were found with (A) rno-miR-133b-3p, rno-miR-378a-3p, and rno-miR-434-3p equally expressed in both muscle types, (B) rno-miR-1-3p and rno-miR-133a-3p with higher expression in EDL and (C) rno-miR-206-3p, mmu-miR-208b-3p, and rno-miR-499-5p with higher expression in SOL. [score:7]
Both miR-208b-3p and -499-5p are expressed almost exclusively in soleus, consistent with the location of their coding DNA within Myh7 (coding for MYH-1) and Myh7b (coding slow-tonic MYH transcribed in slow fibers) (van Rooij et al., 2009). [score:3]
Conversely, miR-206-3p, miR-208-3p, and -499-5p expression was significantly higher in the soleus muscle compared to the EDL (7.4-, 10.7-, and 35.4-fold respectively; Figure 2C). [score:2]
This is further supported by the study of Muroya et al. (2013), where the sequencing read count of bta-miR-1, -133a and -206 are among the most frequently detected miRNAs in bovine skeletal muscles (mean read count of both semitendinous and masseter muscles ranging from ∼1260528 for bta-miR-1 to ∼80481 for bta-miR-206), while bta-miR-208b was detectable but with lower read count (∼1687) (Muroya et al., 2013). [score:1]
Surprisingly, in our previous study we observed that miR-208b-3p and -499-5p were significantly elevated following massive muscle damage induced by a myotoxic injection. [score:1]
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[+] score: 7
For example, miR-208 was up-regulated, while miR-1 and miR-133a were down-regulated in MI [14]. [score:7]
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[+] score: 7
miR-448, let-7b, miR-540, miR-296, miR-880, miR-200a, miR-500, miR-10b, miR-336, miR-30d, miR-208, let-7e, miR-142-5p, miR-874, miR-375, miR-879, miR-501, and miR-188 were upregulated, while miR-301b, miR-134, and miR-652 were downregulated in TMH group (Table 5). [score:7]
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[+] score: 5
Other miRNAs from this paper: rno-mir-92a-1, rno-mir-92a-2, rno-mir-208a, rno-mir-320, rno-mir-494
Similarly, Montgomery et al. found that inhibition of miR-208 was also a potent therapeutic target for modulating cardiac function and remo deling [20]. [score:5]
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[+] score: 5
Notably, cardiac-specific miR-1, miR-133, miR-208 and miR-499 were all suppressed by two or more orders of magnitude [34], [35], as were the stemness and cell cycle repressors miR-141 and miR-137 [36]; in contrast, the proliferative miRNAs, miR-222 [37], increased dramatically in MDCs, and miR-221 was undetectable in myocytes but highly expressed in MDCs (Figure 5D). [score:5]
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[+] score: 4
The results showed that miR-208, miR-124, miR-146a-5p, miR-103, and miR-21 were all expressed abnormally in spinal tissue of ASCI rats (Figure 2). [score:3]
In the ASCI group, the levels of miR-208, miR-124, and miR-146a-5p were decreased, while the levels of miR-103 and miR-21 were increased. [score:1]
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[+] score: 4
Reports have shown that miR-208 and miR-140 affect their host genes 25, 26; however, miR-26 suppresses its host gene to regulate neurogenesis [27]. [score:4]
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[+] score: 3
Other specifically expressed miRNAs that we verified are mir-208, which is known to be restricted to the heart [47] and mir-122, the most prominent miRNA in liver [48]. [score:3]
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[+] score: 3
Interestingly, the miR-133 family, together with miR-1, miR-206 and miR-208, is specifically expressed in muscle; thus, these miRNAs are called myomiRs 42. [score:3]
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[+] score: 2
It has been observed that many miRNAs regulate cell apoptosis, such as miR-1, miR-133, miR-199, miR-208, miR-320, miR-21, and miR-204, etc [18- 23]. [score:2]
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[+] score: 2
Several candidate therapeutic miRNAs have progressed into clinical and preclinical development; for example, antisense miR-122 is being developed as a treatment for hepatitis C virus, miR-208/499 for chronic heart failure, miR-195 for myocardial infarction and miR-34 and let-7 for cancer 10, 11. [score:2]
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[+] score: 2
Groups of tissue-specific (e. g., miR-1, miR-206, miR-208) and non-tissue-specific (e. g., miR-29a, miR-23a) microRNAs have been found to control skeletal muscle development in growth and differentiation [13]– [19]. [score:2]
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[+] score: 2
Bostjancic E Zidar N Stajer D MicroRNAs miR-1, miR-133a, miR-133b and miR-208 are dysregulated in human myocardial infarctionCardiology. [score:2]
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[+] score: 2
It has also been reported that plasma levels of some miRNAs (mir-1, mir-208, mir-133a, mir-423-5p, mir-499) can be used as biomarkers for myocardial injury [90– 92]. [score:1]
Recent studies have shown that cardiac muscle-rich miRNAs or myomiRNAs such as mir-208 (mir-208a, b) play crucial roles in CVD [85– 87]. [score:1]
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[+] score: 2
For instance, miR-208 is a heart-specific miRNA that is released into the blood stream from injured cardiomyocytes [3]. [score:1]
1997.3477 9087178 3. Ji X Plasma miR-208 as a biomarker of myocardial injuryClin Chem. [score:1]
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[+] score: 2
9 -45.6 mmu-miR-27b -1.8 -71.4 -462.7 mmu-miR-214* -2.6 -5.0 -43.5 mmu-let-7c-1* -73.2 -204.4 -334.1 mmu-miR-34c -9.4 -26.1 -42.7 mmu-miR-542–3p -5.9 -195.6 -319.8 mmu-miR-706 -9.3 -5.0 -38.7 mmu-miR-487b -2.0 -161.5 -263.9 mmu-miR-467b* -10.1 -2.2 -33.6 rno-miR-17–3p -1.6 -152.0 -248.5 mmu-miR-323–3p -3.7 -23.3 -29.8 mmu-miR-10b -2. 4 -136.6 -223.3 mmu-miR-202–3p -6.5 -5.9 -21.4 mmu-miR-29b -3.0 -135.1 -220.9 mmu-miR-339–5p -1.6 -9.6 -19.6 mmu-miR-297a* -2.4 -128.4 -209.8 mmu-miR-181c -2.0 -10.5 -14.6 mmu-miR-692 -41.5 -115.8 -189.2 mmu-miR-203 -4.6 -6.4 -13.8 mmu-miR-208 -40.6 -113.5 -185.5 mmu-miR-467a* -2.6 -3.9 -11.4 mmu-miR-467c -38.9 -108.6 -177. [score:1]
Among other miRNA such as miR-208 is associated with adverse clinical outcomes in human dilated cardiomyopathy [32]. [score:1]
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[+] score: 1
A few miRNAs are found to be enriched in the heart including miR-1, miR-133, miR-208a, miR-208b, and miR-499. [score:1]
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[+] score: 1
Other miRNAs from this paper: rno-mir-34b, rno-mir-34c, rno-mir-34a, rno-mir-208a
Only two studies had attempted to identify circulating miR-208 as a marker for DOXO-cardiotoxicity in breast cancer patients and in an animal mo del, but both failed to demonstrate their intention [46, 47]. [score:1]
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[+] score: 1
Dozens of miRNAs have been identified in myocardial cells, including miR-133a, miR-133b, miR-1d, miR-296, miR-21, miR-208 and miR-195 (4– 18). [score:1]
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[+] score: 1
MicroRNA profiling identified several miRNAs that have been previously associated with cardiac hypertrophy such as miR-214, miR-23b, miR-15b, rno-miR-26b, rno-miR-221, rno-miR-222, rno-miR-107 [59], miR-23a, miR-208, rno-miR-133b, miR-19a and mi-r133a [60]. [score:1]
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[+] score: 1
And 2 non-PRmiRs let-7f and miR-208 did so. [score:1]
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[+] score: 1
Other important myomiRs, namely miR-208b, miR-486 and miR-499, have been identified [17]. [score:1]
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[+] score: 1
Likewise, a combination of miR-1, miR-133, miR-208 and miR-499 is capable of reprogramming fibroblasts into cardiomyocytes [21]. [score:1]
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[+] score: 1
Other miRNAs from this paper: hsa-mir-208b
Despite knowledge of the impact of motor-nerve impulse frequency [2– 6] and the complex transcriptional circuitry including peroxisome proliferator-activated receptor (PPAR) α, δ, PPARγ coactivator1 (PGC1), and miR208b/499 elements in muscle fibers [7– 14], the molecular mechanisms modulating fiber-type composition are not clearly understood. [score:1]
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[+] score: 1
With these criteria we identified eight miRNAs: miR-140-3p, miR-140-5p,,, miR-208b-3p,, miR-743b-5p, and miR-879-3p (Table  1). [score:1]
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[+] score: 1
Cycling acute or chronic exercise did not change the serum levels of muscle-enriched miRNAs (miR-1, miR-133a, miR-133b, miR-206, miR-208b, miR-486, and miR-499) with an exception for miR-486, which showed a significant negative correlation with VO [2max] (Pedersen et al., 2007). [score:1]
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[+] score: 1
For example, miRNAs involved in cardiac hypertrophy and heart failure such as miR-208, miR-133, miR-195, miR-21, and miR-126 have been reported in several studies [5- 8]. [score:1]
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