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70 publications mentioning mmu-mir-208b

Open access articles that are associated with the species Mus musculus 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.

1
[+] score: 155
Myostatin, a target gene of microRNA-208b and microRNA-499-5p and an inhibitor of muscle growth, is upregulated and inversely correlated with the expression of these microRNAs. [score:10]
Correlation between (C) MYH7 gene expression and microRNA-208b expression and (D) MYH7b gene expression and microRNA-499-5p expression in people with spinal cord injury and able-bodied control subjects. [score:9]
Correlation between (C) myostatin gene expression and microRNA-208b expression and (D) myostatin gene expression and microRNA-499-5p expression in people with spinal cord injury and able-bodied controls. [score:9]
Expression of microRNA-208b and microRNA-499-5p is decreased after spinal cord injury and correlates with expression of host genes MYH7 and MYH7bExpression of microRNA-208b and microRNA-499-5p progressively declined with time after spinal cord injury (Fig. 2). [score:7]
Direct modulation of gene target expression was studied in vivo by gene transfer of microRNA-208b or microRNA-499-5p in intact mouse muscle by electroporation. [score:6]
Our findings corroborate earlier studies describing a feedback loop regulating skeletal muscle mass (McCarthy et al. 2009; van Rooij et al. 2009), whereby decreased expression of MYH7 and MYH7b attenuate the expression of the encoded myomirs, microRNA-208b, and microRNA-499-5p. [score:6]
We also report that in vivo overexpression of microRNA-208b, but not microRNA-499-5p directly reduced myostatin gene expression in mouse skeletal muscle. [score:6]
Myostatin expression was inversely correlated with microRNA-208b and microRNA-499-5p expression in all groups (r =  0.702 and 0.637, respectively, P < 0.001, Fig. 3C– D). [score:5]
Furthermore, expression of both microRNA-208b and microRNA-499-5p correlated with expression of their respective host genes, namely MYH7 and MYH7b (r =  0.810 and 0.656, respectively, P <  0.001 Fig. 2C-D). [score:5]
Overexpression of microRNA-208b in mouse skeletal muscle decreases myostatin gene expression. [score:5]
Finally, overexpression of microRNA-208b, but not microRNA-499-5p, in adult rodent skeletal muscle decreased myostatin gene expression. [score:5]
In individuals with long-standing injury, microRNA-208b expression declined to 3% of that observed in the able-bodied control group (P < 0.001), with expression levels being close to the limit of detection. [score:5]
Here, we demonstrate that overexpression of microRNA-208b, though not microRNA-499-5p, in rodent skeletal muscle decreased myostatin gene expression in vivo. [score:5]
Expression of microRNA-208b and microRNA-499-5p is decreased after spinal cord injury and correlates with expression of host genes MYH7 and MYH7b. [score:5]
Relative mRNA expression of myostatin decreased in skeletal muscle overexpressing microRNA-208b, but not microRNA-499-5p (Fig. 4C– D). [score:5]
Collectively, our results provide evidence to suggest that microRNA-208b plays a role in inducing myostatin expression after spinal cord injury in humans and may contribute to the complex regulation of skeletal muscle atrophy in tetraplegia. [score:4]
Thus, the feedback loop is complex and alterations in microRNA-208b can also directly affect myostatin gene expression. [score:4]
While acute and chronic electrical stimulation training consistently increases MYH7, expression of its intronic microRNA-208b have not been assessed. [score:3]
Here, we report that skeletal muscle expression of microRNA-208b and microRNA-499-5p, as well as their host genes MYH7 and MYH7b, decline progressively during the first year after cervical spinal cord injury in humans, with changes maintained in long-standing injury. [score:3]
Thus, we determined the expression of microRNA-208b, microRNA-499-5p, and myostatin in skeletal muscle obtained from people with complete spinal cord injury. [score:3]
The genes encoding slow-twitch oxidative type I muscle fiber myosin heavy chains, MYH7 and MYH7b, intronically express microRNA-208b and microRNA-499-5p, respectively (McCarthy et al. 2009). [score:3]
Although myostatin has been validated as a target of both microRNA-208b (Callis et al. 2009) and microRNA-499-5p by luciferase assay (Bell et al. 2010), the in vivo regulation is unknown. [score:3]
Hindlimb suspension for 28 days leads to skeletal muscle atrophy, concomitant with decreased expression of microRNA-208b and microRNA-499-5p in rat soleus muscle (McCarthy et al. 2009). [score:3]
Expression of microRNA-208b and microRNA-499-5p, as well as the slow myosin genes to which these particular microRNAs are intronic, decline progressively within the first year after spinal cord injury. [score:3]
MicroRNA-208b and microRNA-499-5p have similar seed regions that overlap by six bases, indicating that they share several target genes (van Rooij et al. 2009). [score:3]
The myostatin 3′ untranslated region (UTR) includes a mouse to human conserved seed -binding site for microRNA-208b and microRNA-499-5p (Fig. 3A). [score:3]
MicroRNA-208b and microRNA-499-5p have nearly identical seed sequences and therefore share many predicted gene targets. [score:3]
Moreover, myostatin expression was inversely correlated with microRNA-208b and microRNA-499-5p in human skeletal muscle following spinal cord injury, coincident with skeletal muscle atrophy. [score:3]
In conclusion, skeletal muscle expression of microRNA-208b and microRNA-499-5p progressively declined within the first year after cervical spinal cord injury in humans, with changes maintained in long-standing injury. [score:3]
Figure 4(A) Expression of microRNA-208b in mouse skeletal muscle after electroporation with either microRNA-208b or a control plasmid. [score:3]
Expression of microRNA-208b and microRNA-499-5p progressively declined with time after spinal cord injury (Fig. 2). [score:3]
In particular, microRNA-208b and microRNA-499-5p play a role in the regulation of skeletal muscle fiber type and skeletal muscle mass (McCarthy et al. 2009; van Rooij et al. 2009). [score:2]
MicroRNA-208b expression was decreased ∼35% and ∼80% at months 3 and 12 after injury, respectively, compared to the able-bodied control group (P < 0.02 and P < 0.001, Fig. 2A). [score:1]
Intact tibialis anterior mouse muscle was electroporated with either a control plasmid or plasmid encoding for pri-microRNA-208b or pri-microRNA-499-5p. [score:1]
Moreover, mice lacking both microRNA-208b and microRNA-499-p5 show a substantial loss of slow-twitch myofibers (van Rooij et al. 2009). [score:1]
Tibialis anterior muscles of adult C57Bl/6J mice were electroporated with either a control plasmid or plasmid encoding for pri-microRNA-208b or pri-microRNA-499-5p (Origene, Rockville, MD) as described previously (Kulkarni et al., 2011). [score:1]
The so-called myomir family is a group of microRNAs that includes microRNA-208a, microRNA-208b, and microRNA-499-5p, which fine-tune muscle morphology and function (McCarthy 2011). [score:1]
Nevertheless, the role of microRNA-208b and microRNA-499-5p in the control of protein synthesis in human skeletal muscle has yet to be determined. [score:1]
Given the known role of microRNA-208b and microRNA-499-5p in determining skeletal muscle size in rodents (van Rooij et al. 2009), we hypothesized that they may be altered, concomitant with skeletal muscle atrophy, in humans after spinal cord injury. [score:1]
Figure 3(A) Predicted microRNA seed/mRNA 3′-UTR interaction between microRNA-208b and microRNA-499-5p within the 3′-UTR of the human and mouse myostatin transcripts according to microRNA. [score:1]
Whether microRNA-208b and microRNA-499-5p contribute to skeletal muscle atrophy in spinal cord injury is unknown. [score:1]
With this method, we achieved an overexpression of microRNA-208b or microRNA-499-5p in predominantly glycolytic, type II, tibialis anterior muscle, respective to control muscle (Fig. 4A– B) that was comparable to levels measured in nontransfected oxidative soleus muscle (data not shown). [score:1]
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2
[+] score: 48
Other miRNAs from this paper: mmu-mir-499
Downregulation of miR-208b Expression in Vgll2 Deficient Skeletal Muscle and Increase in its Target Proteins. [score:8]
At P7, consistent with gene expression results of their host MyHC mRNAs (Fig.   2), the expression level of miR-208b was significantly reduced in Vgll2 [−/−] GPS muscles by 39%, whereas miR-499 expression was slightly increased (Fig.   6). [score:7]
As miR-208b uses the Myh7 promoter [21], the Vgll2-TEAD1 complex may also regulate miR-208b expression through Myh7 promoter regulation. [score:5]
Interestingly, miR-208b, which works as a slow type regulator in a miRNA -mediated transcriptional regulatory network, was also decreased in the GPS muscles of Vgll2 [−/−] neonates in parallel with Myh7 expression. [score:5]
In this study, we found that Vgll2 -deficient mice exhibited a faster muscle contractile phenotype under basal conditions and significant expression changes of Myh7/miR-208b and its downstream targets of transcriptional repressor proteins for slow-twitch fiber in neonatal skeletal muscles. [score:5]
Although these miRNAs share a comparable seed sequence and target the same mRNAs, they are differentially regulated: miR-208b is encoded within the Myh7 gene, and miR-499 is encoded within Myh7b gene [43]. [score:4]
The Absence of Vgll2 results in shifts in fiber type of skeletal muscle toward a faster phenotype and decreases in slow isoform MyHC gene and its intronic miRNA, Myh7/miR-208b, and deregulation of miR-208b targets. [score:4]
miR-208b and miR-499 expression levels in the GPS muscle from Vgll2 [+/+] and Vgll2 [−/−] mice at P7 (n = 8). [score:3]
Previous studies showed that two miRNAs, miR-208b and miR-499, serve as fiber-type modulators by inhibiting the activity of transcriptional repressors of genes encoding slow-twitch contractile proteins such as Sox6, Sp3, and Purβ 21, 39– 42. [score:3]
miR-208b represses negative regulators of slow-twitch muscle genes such as Sox6, Sp3, and Purβ [21]. [score:2]
In order to further validate the reduction in miR-208b in Vgll2 [−/−] skeletal muscles, we compared protein levels of its downstream targets, Sox6, Sp3, and Purβ by Western blotting analysis. [score:2]
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3
[+] score: 28
Other miRNAs from this paper: mmu-mir-208a, mmu-mir-16-1, mmu-mir-16-2
MiR-208a inhibits the Sox6 factor, which inhibits the expression of both β-MyHC and miR-208b [11], [12]. [score:7]
In rodent heart, alpha-Myosin Heavy Chain (MyHC) and its micro -RNA miR-208a regulate the expression of beta-MyHC and of its intronic miR-208b. [score:4]
Indeed, the maintained expression of miR-208a and the strong induction of miR-208b mRNA in Ren mice (Figure 5B and C) was in agreement with the low Sox6 mRNA level (−50%, p0.05 vs. [score:3]
Interestingly, in AS-Ren mice the increase of miR-208b transcription that was observed in Ren mice was significantly inhibited (−60% vs. [score:3]
Furthermore, in AS-Ren mice the expression profiles of miR-208a, Sox6, miR-208b (Figure 5 A, C and B) and of β-MyHC (Figure 2D) were reversed by eplerenone (+250%, −50%, +221%, +242%, respectively, vs. [score:3]
As expected in the experimental groups, the expression of miR-208b (x3.8; p<0.01 vs. [score:3]
Effect of combined cardiac aldosterone and hypertension on cardiac miR-208 and Sox6 expression. [score:3]
Similarly, the Myh7 gene encodes β-MyHC and miR-208b. [score:1]
Besides, the AH -induced increase of ßMyHC and its intronic miRNA-208b was prevented in AS-Ren. [score:1]
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4
[+] score: 27
A dual-detargeted virus named vMC [24]-NC, with miR-124 targets in the 5′ NCR and miR-133 plus miR-208 targets in the 3′ NCR, showed the suppression of replication in both nervous and cardiac tissues but retained full oncolytic potency when administered by intratumoral (10 [6] 50% tissue culture infectious doses [TCID [50]]) or intravenous (10 [7] to 10 [8] TCID [50]) injection into BALB/c mice bearing MPC-11 plasmacytomas. [score:9]
In vivo toxicity testing confirmed that miR-124 targets within the 5′ NCR suppressed virus replication in the central nervous system while miR-133 and miR-208 targets in the 3′ NCR suppressed viral replication in cardiac tissue. [score:9]
To enhance its safety profile, microRNA target sequences complementary to miR-124 or miR-125 (enriched in nervous tissue), miR-133 and miR-208 (enriched in cardiac tissue), or miR-142 (control; enriched in hematopoietic tissues) were inserted into the vMC [24] NCRs. [score:3]
This inhibition of viral replication by the 3′ NCR insertions may be due to the presence of miR-142, miR-133, or miR-208 in certain cells or nonspecific effects of the insertions themselves. [score:3]
Unexpectedly, mice injected with vMC [24]-H2 or vMC [24]-C also had reduced mean viral loads in all three tissues, suggesting that either the placement of the insert can control viral replication in vivo or that there are low to intermediate levels of miR-142, miR-133, or miR-208 present regulating viral tropism. [score:2]
Sequences complementary to miR-142, miR-124, miR-125, miR-133, and miR-208 were successfully incorporated (individually or in combination) into the 5′ and 3′ NCRs of the vMC [24] genome. [score:1]
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5
[+] score: 25
Distinct groups of miRNAs regulated by IAV infection could be defined: (1) miRNAs (n = 39) whose expression correlated with hemagglutinin (HA) mRNA expression and represented the general response to IAV infection independent of host genetic background; (2) miRNAs (n = 20) whose expression correlated with HA mRNA expression but differed between the two strains; and (3) remarkably, miR-147-3p, miR-208b-3p, miR-3096a-5p, miR-3069b-3p, and the miR-467 family, whose abundance even in uninfected lungs differentiated nearly perfectly (area under the ROC curve > 0.99) between the two strains throughout the time course, suggesting a particularly strong association with the differential susceptibility of the two mouse strains. [score:10]
Before infection, host susceptibility was particularly associated with consistently higher expression of miR-208b-3p, miR-3096b-3p, and the miR-467 family and lower expression of miR-3096a-5p and the potentially anti-inflammatory miR-147-3p. [score:5]
Taken together, the above results suggest (1) that the selective expression of several IAV-regulated miRNAs, including miR-147-3p, miR-208b-3p, miR-3096a-5p, miR-3069b-3p, and the miR-467 family, in uninfected and incipiently infected DBA/2J lungs was specifically associated with higher susceptibility of this mouse strain to IAV infection at later time points and (2) that it accurately predicted this higher susceptibility. [score:4]
In total, there were eight differentially expressed miRNAs with AUCs > 0.99 (miR-147-3p, miR-208b-3p, miR-467a-5p, miR-467c-5p, miR-467d-5p, miR-467e-5p, miR-3096a-5p, and miR-3096b-3p) whose abundance changed significantly during infection. [score:3]
Out of these, miR-208b-3p, miR-467b-5p, miR-345-3p, and miR-744-3p were differentially expressed during infection in both mouse strains. [score:3]
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6
[+] 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]
[1 to 20 of 10 sentences]
7
[+] 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, 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-208b, 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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8
[+] score: 21
Based on this observation, we combined the analysis from the TF gene coexpression network of TF genes and miRNAs and hypothesized that the functions related to cardiac hypertrophy were induced by the up-regulated TF genes in Module 1 at days 3 and 5 but suppressed by some miRNAs after day 7. Runt related transcription factor 1 (Runx1), for example, in Module 1 is a key regulator of heart post-myocardial infarction [24] and was up-regulated from day 3 to day 14 and likely suppressed by some known cardiac miRNAs, such as miR-126–5p, miR-195, miR-208b, and miR-21 at day 28 (Suppl. [score:14]
Moreover, Toll-like receptor 2 (Tlr2), a regulator involved in the signaling pathway of cardiomyocyte dysfunction and inflammatory responses [26], also in Module 1, was up-regulated at day 7 and then likely suppressed by miR-208b at days 14 and 28. [score:7]
[1 to 20 of 2 sentences]
9
[+] score: 20
For example, miR-208, miR-9, let-7a, 7b, and miR-22* were found to be up-regulated in transformed IEC-6 cells, whereas miR-539, miR-181d, and miR-146a were down-regulated. [score:7]
Consistent with the specific expression of MHC in the heart and the pulmonary myocardium, miR-208 is expressed specifically in the heart and at trace levels in the lung [33]. [score:5]
Among these differentially expressed miRNAs, we verified the alteration of miR-208 and miR-22*. [score:3]
So the expression of miR208 and miR22* was chosen to be validated. [score:3]
miR-208 is encoded by intron 27 of the human and mouse MHC gene. [score:1]
The relationship between miR-208 and tumorigenesis was not clear and needed further study. [score:1]
[1 to 20 of 6 sentences]
10
[+] score: 19
Other miRNAs from this paper: mmu-mir-208a, mmu-mir-499, dre-mir-499
The increased transcription of Myh6 and Myh7 in Sox6 KO muscle, therefore, could lead to upregulation of miR-208, which in turn, suppress fast fiber specific gene expression. [score:8]
It has been reported that miR-208 suppresses expression of THRAP1, which promotes fast fiber specific gene expression [96]. [score:7]
It should be noted that miR-208, along with miR-499, also targets the 3'-UTR region of Sox6 [68, 97, 98]. [score:3]
In the intron sequences of Myh6 and Myh7, miR-208a and miR-208b are encoded, respectively [95]. [score:1]
[1 to 20 of 4 sentences]
11
[+] score: 17
IPost up-regulated miR-1, miR-15b, miR-21, miR-24, miR-26a, miR-27, miR-133a, miR-199a, miR-214, miR-208 and miR-499, while down-regulated miR-23a and miR-9 as compared with Sham group. [score:6]
Compared with sham group, the expressions of miR-1, miR-15b, miR-21, miR-24, miR-26a, miR-27, miR-133a, miR-199a, miR-214, miR-208 and miR-499 were increased in IPost hearts, while miR-9 and miR-23a were down-regulated in IPost mo dels. [score:5]
Then real-time quantitative PCR was performed to quantify the expression level of miR-1, miR-9, miR-15b, miR-21, miR-23a, miR-24, miR-26a, miR-27, miR-133a, miR-199a, miR-208, miR-214 and miR-499 with SYBR Green PCR Master Mix (Applied Biosystems) according to the manufacturer’s instructions. [score:3]
As previously reported, a collection of miRNAs were abnormally expressed in ischemic mouse hearts in response to I/R injury, such as miR-1, miR-9, miR-15b, miR-21, miR-23a, miR-24, miR-26a, miR-27, miR-133a, miR-199a, miR-208, miR-214 and miR-499 [20, 21, 28]. [score:3]
[1 to 20 of 4 sentences]
12
[+] score: 17
The previous studies indicate that miR-208-3p is dysregulated in some cardiovascular and muscular diseases [16– 18]. [score:4]
In agreement with our hypothesis, miR-208-3p has also been shown to be upregulated and behave as an oncogenic miRNA in these human tumor types. [score:4]
miR-208 is wi dely known to play a critical role in the formation of cardiovascular and muscular diseases [16– 18]. [score:3]
However, there are few studies exploring the expression and function of miR-208-3p in cancers, except some occasional reports in pancreatic cancer [19], esophageal squamous cell carcinoma [20], hepatocellular carcinoma [21] and prostate carcinoma [22]. [score:3]
However, miR-208 has also been reported to be involved in human cancers occasionally, including pancreatic cancer [19], esophageal squamous cell carcinoma [20], hepatocellular carcinoma [21] and prostate carcinoma [22]. [score:1]
Future research emphasis is needed to characterize the feasibility of targeting miR-208-3p in gastric cancer therapy and developing simplified and cost-effective manipulation methods. [score:1]
One such example is miR-208. [score:1]
[1 to 20 of 7 sentences]
13
[+] score: 15
Other miRNAs from this paper: hsa-mir-499a, hsa-mir-208b
Specifically, HCV was found to regulate expression of two microRNAs (miR-208b and miR-499a-5p) that target the 3′ untranslated region (UTR) of IFNL3 leading to its degradation, allowing for viral persistence. [score:8]
Intriguingly, these same microRNAs also dampen type I IFN signaling in HCV-infected hepatocytes by downregulating expression of IFNAR1, a mechanism distinct from miR-208b and miR-499a-5p regulation of type III IFN (104). [score:7]
[1 to 20 of 2 sentences]
14
[+] score: 13
It has been shown that miRNAs are determinants of the physiology and pathophysiology of the cardiovascular system and altered expression of muscle- and/or cardiac-specific miRNAs such as the miRNAs named miR-1, miR-208 and miR-133 in myocardial tissue is involved in heart development and cardiovascular diseases, including myocardial hypertrophy, heart failure and fibrosis [11– 14]. [score:6]
Although, this study focus in the acute phase of the experimental Chagas disease some miRNAs (miR-133, miR-208) were found down regulated at 45 dpi in accordance with previously reported in human heart of Chagas chronic patients [15]. [score:4]
In the study, we have found that the same muscle- and/or cardiac-specific miRNAs, miR-1, miR-133 and miR-208 were downregulated in CCC myocardium as compared to control myocardium [15]. [score:3]
[1 to 20 of 3 sentences]
15
[+] score: 12
Other miRNAs from this paper: hsa-mir-499a, mmu-mir-499, hsa-mir-208b, hsa-mir-499b
MiR-208b is encoded within an intron of the Myh7 gene, such that an increase in miR-208b expression could also result in an increase in Myh7 expression due to the fact that they are co-regulated [50]. [score:6]
This apparent disconnect between DNA methylation status and gene expression level for Myh7 may be explained in part by the fact that the promoter region for miR-208b was hypomethylated. [score:3]
Of the miRNA promoter regions with DMRs, two were related to cardiac hypertrophy including miR-208b and miR-499 (Table 8) [49], [50]. [score:1]
However, unlike Myh7 which was hypermethylated, regions within the promoter for both miR-208b and miR499 were hypomethylated. [score:1]
MiR-208b is located within intron 31 of the Myh7 gene which is also differentially methylated and miR-499 is located in intron 19 of Myh7b. [score:1]
[1 to 20 of 5 sentences]
16
[+] score: 11
Other miRNAs from this paper: mmu-mir-301a, hsa-mir-301a, hsa-mir-20b, mmu-mir-20b, hsa-mir-208b
[28] The two downregulated miRNAs, miR-208b-3p induced apoptosis in myocardial cell, [29] however, the role of miR-301a-5p in apoptosis remains unclear (Figure 4b). [score:4]
The expression of miR-208b-3p, miR-301a-5p, miR-1273g-3p and miR-20b-3p was confirmed by real-time PCR (Figure 4c), which is consistent with microarray analysis. [score:3]
[28] The expression levels of miR-208b-3p and miR-301a-5p were consistently high in VAN group, which was decreased in siRNA MBD2 with VAN group. [score:3]
A recent study reported that miR-208b-3p might promote apoptosis in myocardial cell. [score:1]
[1 to 20 of 4 sentences]
17
[+] score: 10
Two further examples are Mir208a and Mir208b, which are located in introns of Myh6 and Myh7 respectively and are differentially expressed in parallel with their host gene expression in mouse heart, suggesting that the miRNAs are processed from the intronic transcript rather than being transcribed as a separate RNA [40,41]. [score:5]
miR-208 knockout mice display a reduced hypertrophic response to thoracic aortic banding, and this microRNA is thought to regulate stress -dependent gene expression in the heart [40] and is required for normal cardiac conduction [41]. [score:5]
[1 to 20 of 2 sentences]
18
[+] score: 10
Our group has observed dysregulated miRNA expression in heart samples from CCC patients [21] and acute T. cruzi infection in mice [33] including miR-133 and miR-208, which regulate heart genes related to cardiovascular disease 34– 39. [score:7]
Satoh M Minami Y Takahashi Y Tabuchi T Nakamura M Expression of microRNA-208 is associated with adverse clinical outcomes in human dilated cardiomyopathyJ Card Fail. [score:3]
[1 to 20 of 2 sentences]
19
[+] score: 9
0130658.g006 Fig 6 (A) qPCR validation of selected miRs from the microRNA array showing significant down-regulation of miR-21 and miR-92a and significant up-regulation of miR-27, miR-29, miR-208 and miR-214 in CR compared to Ad lib. [score:6]
In addition, miR-27, miR-29, miR-208 and miR-214 were significantly up-regulated in CR as compared to AL groups (+2.969±0.5318, P<0.05; +7.483±1.084, P<0.002; +2.483±0.9468, P<0.009; and +2.003±0.5865, P<0.02; fold change respectively, N = 3) (Fig 6A). [score:3]
[1 to 20 of 2 sentences]
20
[+] score: 9
To test whether the observed cardiac or muscle miRNA expression profiles changes are temporal, we compared the miRNA expression profiles of mice hearts at postnatal days 0, 3, 8, and 14 by using qRT-PCR and found miR-1a-3p, miR-133b-3p, miR-208b-3p, and miR-206-3p were significantly decreased while miR-208a-3p was upregulated (Figure 1). [score:7]
An increasing number of miRNAs with different functions in heart development have also been identified, including miR-1, miR-208, miR-133, miR-206, miR-126, miR-143, miR-145, and miR-499; from this group, we analyzed the 7 miRNAs most relevant to postnatal heart growth. [score:2]
[1 to 20 of 2 sentences]
21
[+] score: 9
In response to calcium signaling, miR-208b and miR-499 indeed reinforce slow fiber conversion by inducing the expression of β-MHC and Myh7b (Van Rooij et al., 2009). [score:3]
Highly expressed miRNAs in skeletal muscle tissue are termed myomiRs, which include miR-1, miR-133a, miR133-b, miR-206, miR-208, miR208b, miR486, and miR-499 (Van Rooij et al., 2008). [score:3]
The fine-tuned expression of miR-499 and miR-208b plays a role in the control of skeletal muscle performance. [score:3]
[1 to 20 of 3 sentences]
22
[+] score: 8
Other miRNAs from this paper: mmu-mir-214
However, a recent study revealed that interaction of EZH2 and primary microRNA-208b (pri-miR-208b) regulates hypertrophic gene expression, and attenuation of EZH2 can restore antisense β-MHC and α-MHC gene expression, and inhibit cardiac hypertrophy 22. [score:8]
[1 to 20 of 1 sentences]
23
[+] score: 8
In recognition that cardiovascular disease and cardiac remo deling is associated with simultaneous dysregulation of several miRNAs (e. g. miR-1, miR-34a, miR-133, miR-199b, miR-320 [11], [15], [36]– [38]) or miRNA families (e. g. miR-34 family [10], miR-208 family [39]), tiny 8-mer seed -targeting LNA-antimiRs could provide an advantage by simultaneous inhibition of entire miRNA seed families [10], [27]. [score:8]
[1 to 20 of 1 sentences]
24
[+] score: 6
The suppression of miR-155 was also discovered the study of the influence of several isoflavones from soy on prostate cancer cell lines, where miR-155, miR-208b, miR-211, miR-376a and miR-411 were found to be downregulated by the isoflavones by more than three to five fold than control cells [32]. [score:6]
[1 to 20 of 1 sentences]
25
[+] score: 6
We performed qPCR to detecct the expression levels of ANF, BNP and several stress-responsive miRNAs (miR-29, miR-195 and miR-208) in Myh6-miR-24 transgenic and control hearts. [score:3]
Similarly, miR-29, miR-195 and miR-208 were dramatically reduced upon MI, but were partially restored by overexpression of miR-24 in cardiomyocytes (Fig. 4K). [score:3]
[1 to 20 of 2 sentences]
26
[+] score: 6
miR-208b and miR-499 were reported to control muscle fiber type by inhibiting fast muscle-specific genes while promoting slow myofiber genes. [score:3]
Our results indicated that starvation induced C2C12 myotubes atrophy led to the secretion of miR-1, miR-23a, miR-133, miR-206, miR-208b, and miR-499 into the culture medium, which could be used as indicators for muscle atrophy. [score:1]
However, the serum profiles of miR-1, miR-133, and miR-208b were different between human and mice, which required further research. [score:1]
However, no significant changes were found in the levels of miR-1, miR-133, and miR-208b following HDBR (Figures 4(a), 4(c), and 4(e)). [score:1]
[1 to 20 of 4 sentences]
27
[+] score: 6
Resolvin D1 upregulates several micro RNAs (miRNAs; e. g., miR-146, miR-219, miR-208) that are involved in NFκB and IL-10 expression in resolution. [score:6]
[1 to 20 of 1 sentences]
28
[+] score: 6
Other miRNAs from this paper: mmu-mir-208a
Previously, our study had found that insulin promotes VSMCs proliferation and migration via microRNA-208 -mediated downregulation of p21 and inducing dopamine D [1] receptor dysfunction, and activation of the dopamine D [4] receptor suppresses the effect of insulin on VSMCs [30– 32]. [score:6]
[1 to 20 of 1 sentences]
29
[+] score: 5
The parallel identification of miR-208 expression, an intronic miR encoded in the cardiac alfa-myosin heavy chain (αMHC) gene, which promotes the transition from the embryonic to adult isoforms of cardiac contractile proteins, further stresses the CSC commitment to the adult cardiomyocyte lineage. [score:3]
The expression of miR-133a, miR-133b and miR-208 is considered a specific mark of cardiomyocyte lineage differentiation [13]– [16]. [score:2]
[1 to 20 of 2 sentences]
30
[+] 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]
[1 to 20 of 1 sentences]
31
[+] 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]
[1 to 20 of 1 sentences]
32
[+] score: 4
In another separate study [49], we reported that miR-499 are strongly associated with cardiac differentiation and share many predicted targets with miR-208 that has been previously shown to associate with cardiac development. [score:4]
[1 to 20 of 1 sentences]
33
[+] score: 4
The expression pattern of miR-208a (C) and miR-208b (D) in these conditions is similar to the pattern of their host genes. [score:3]
MiRNA-208a and miRNA-208b are triggered in thyroid hormone -induced cardiac hypertrophy - role of type 1 angiotensin II receptor (AT1R) on miRNA-208a/α-MHC modulation. [score:1]
[1 to 20 of 2 sentences]
34
[+] score: 4
Several miRNAs are upregulated and associated with tumorigenesis in ESCC, such as miR-21, miR-138, miR-223, miR-92a, miR-9, and mir-208. [score:4]
[1 to 20 of 1 sentences]
35
[+] score: 4
A subset of miRNAs, miR-1, miR-133, miR-206 and miR-208, are either specifically or highly expressed in cardiac and skeletal muscle and are called myomiRs [6, 7, 13]. [score:3]
Among them, miR-1, miR-133, miR-206, miR-208 and miR-499 have been described as muscle specific miRNAs, or myomiRs [6, 13]. [score:1]
[1 to 20 of 2 sentences]
36
[+] score: 4
Targeted deletion of miR-208, while not leading to a developmental defect, blocked the heart's ability to develop a hypertrophic response to stress [16]. [score:4]
[1 to 20 of 1 sentences]
37
[+] score: 4
qPCR confirmation of exosome-specific expression on miR-10b and miR-208. [score:3]
To validate these data we performed qPCR with pre-amplification cycle for two exosome-specific miRNAs, miR-10b and miR-208. [score:1]
[1 to 20 of 2 sentences]
38
[+] score: 4
This may reflect the challenge of detecting the early stages of miRNA downregulation, particularly for stable mature miRNAs such as miR-208 that has a half-life of >12 days [28]. [score:4]
[1 to 20 of 1 sentences]
39
[+] score: 4
Many miRNAs, such as miR-1, miR-133, miR-29, miR-214, miR-206, miR-486, miR-208b, and miR-499 were involved in the regulation of skeletal myogenesis by binding to its target genes 36, 37. [score:4]
[1 to 20 of 1 sentences]
40
[+] score: 4
F-G Bar graphs showing the expression level of miR-1 (F) and miR-208 (G) in study groups (n = 5 at each time point). [score:3]
Akt was decreased (Figure  4B) and miR-1 (Figure  4C) and miR-208 (Figure  4D) was increased in both the diabetic groups with no significant difference between genders, although there was a trend for increased levels of miR-1 in female diabetics (Figure  4C). [score:1]
[1 to 20 of 2 sentences]
41
[+] score: 3
In addition to the finding that miRNAs as a whole are essential to proper muscle formation, individual miRNAs have been shown to play key roles in myogenesis, including species that regulate satellite cell quiescence (miR-489, [6]), promote proliferation (miR-133, miR-27 [7, 8]), promote myoblast differentiation (miR-206, miR-1, miR-486 [9– 11]), and regulate fiber type switching (miR-499, miR-208a, miR-208b [12]). [score:3]
[1 to 20 of 1 sentences]
42
[+] score: 3
The 10 most inhibited miRNAs are miR-1a, miR-133a/b, miR-196a, miR-206, miR-208b, miR-211, miR-592, miR-653, and miR-1963. [score:3]
[1 to 20 of 1 sentences]
43
[+] score: 3
We also noted that HL-1 cells expressed higher levels of miR-208a than miR-208b, seen as a marker of adult rather than embryonic cardiac tissue [1]. [score:3]
[1 to 20 of 1 sentences]
44
[+] score: 3
Other miRNAs from this paper: mmu-mir-208a
Recent breakthrough data show for the first time that modulation of a single cardiac signaling pathway have profound effects on global energy homeostasis: inhibition of miR-208 in the heart of mice confers resistance to high-fat diet -induced obesity, and improves systemic insulin sensitivity and glucose tolerance [39]. [score:3]
[1 to 20 of 1 sentences]
45
[+] score: 3
Several microRNAs, including miR-1, miR-133, miR-206 and miR-208 [17]– [29], are found in cardiac and/or skeletal muscle, and each has a potentially distinct regulatory function. [score:2]
Evaluation of genes reported to be dysregulated in miR-208a mutant mice revealed elevated levels of Egr1, Egr2, and Fos in the heart, suggesting a potential relationship between miR-499 and miR-208 in regulation of the immediate early gene response to cardiac stress. [score:1]
[1 to 20 of 2 sentences]
46
[+] score: 3
For example, miRNA-21, miRNA-23a, miRNA-24, miRNA-133, miRNA-208/miRNA-195 and miRNA-199 have been shown to be involved in cardiac hypertrophy (15- 17), miRNA-1 in arrhythmia (18), miRNA-29 and miRNA-21 in cardiac fibrosis (19, 20), miRNA-210 and miRNA-494 in ischemic heart disease (21) and miRNA-129 in heart failure (22). [score:3]
[1 to 20 of 1 sentences]
47
[+] 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]
[1 to 20 of 1 sentences]
48
[+] score: 3
However, the expression of both OVOL TFs resulted in the induction of miR-429, miR-208 and miR-200c. [score:3]
[1 to 20 of 1 sentences]
49
[+] score: 3
Some of these microRNAs that exhibit specific patterns of muscle expression are dubbed “myomiRs”; these include members of the bicistronic miR-1/133a and miR206/133b families [20], and a group of microRNAs, namely miR-208, miR-208b, and miR-499, that are embedded in genes encoding the myosin heavy chain [21]. [score:3]
[1 to 20 of 1 sentences]
50
[+] score: 2
Corsten MF Circulating MicroRNA-208b and MicroRNA-499 reflect myocardial damage in cardiovascular diseaseCirc Cardiovasc Genet. [score:2]
[1 to 20 of 1 sentences]
51
[+] score: 2
Other miRNAs from this paper: mmu-mir-1a-1, mmu-mir-1a-2, mmu-mir-1b
MiR-208b is a muscle-specific miR, and plays redundant roles in the specification of muscle fiber identity by activating slow, and repressing fast myofiber gene programs [19]. [score:1]
It is interesting to note that there is a miR-208b binding site in the antisense strand of FoxO3a (data not shown). [score:1]
[1 to 20 of 2 sentences]
52
[+] score: 2
Li H Zheng D Zhang B Liu L Ou J Chen W Xiong S Gu Y Yang J Mir-208 promotes cell proliferation by repressing SOX6 expression in human esophageal squamous cell carcinomaJ Transl Med. [score:2]
[1 to 20 of 1 sentences]
53
[+] score: 2
In addition, recent studies have implicated regulation of several microRNAs (miRNAs) in hypertrophy, including miR-1, miR-133, and miR-208 [11], [12], [13]. [score:2]
[1 to 20 of 1 sentences]
54
[+] score: 1
Both miR-208b and miR-449 have been shown to be highly elevated by cardiovascular damage [41], while several plasma miRNAs have been shown to be specifically affected by drug -induced liver damage [42]. [score:1]
[1 to 20 of 1 sentences]
55
[+] score: 1
Quantitative RT-PCRs using Sybr Green or TaqMan (Invitrogen) for s-RNYs, cel-miR-39, miR-24, miR-17, miR-92a, miR-126, miR-133, miR-145, miR-155, RNU48, and miR-208 were performed on a StepONE system (Applied Biosystem). [score:1]
[1 to 20 of 1 sentences]
56
[+] score: 1
Two other important cardiac miRNAs, mir-208a and mir-208b, do not exist in zebrafish. [score:1]
[1 to 20 of 1 sentences]
57
[+] score: 1
Plasma miR208b and miR449 have been shown to be highly elevated by cardivascular damage [42]. [score:1]
[1 to 20 of 1 sentences]
58
[+] score: 1
Other miRNAs from this paper: hsa-mir-208a, mmu-mir-208a, hsa-mir-208b
We have shown recently that Neb–induced resistance to weight gain in leptin resistant rats involves the cardiac miR-208-MED13 axis [21]. [score:1]
[1 to 20 of 1 sentences]
59
[+] score: 1
Among the differentially expressed microRNAs were miR-181a, miR-208-5p or miR-499, miR-130a, miR-26a and miR-30c with previously characterised functions in skeletal muscle. [score:1]
[1 to 20 of 1 sentences]
60
[+] score: 1
The latter is supported by the observation that the two known miRNAs involved in fast-to-slow fiber programs, miR-208b and miR-499 [48], were not affected in SOD1-G93A mo del (although miR-208b was found to be slow-twitch enriched in both mutant and control animals, Tables S3 and S4). [score:1]
[1 to 20 of 1 sentences]
61
[+] score: 1
Other miRNAs from this paper: mmu-mir-208a, mmu-mir-328, mmu-mir-223, mmu-mir-664
miR-208. [score:1]
[1 to 20 of 1 sentences]
62
[+] score: 1
Among miRNAs expressed in the heart, miR-1, miR-133, miR-208, and miR-499 are the most commonly investigated subtypes. [score:1]
[1 to 20 of 1 sentences]
63
[+] score: 1
A group of miRNAs, highly enriched in skeletal muscle (referred to as myomiRs), has recently been identified and includes miR-1, miR-133a, miR-133b, miR-206, miR-208, miR-208b, miR-486, and miR-499 [33– 37]. [score:1]
[1 to 20 of 1 sentences]
64
[+] score: 1
Additionally, seven miRNAs exhibited a consistent pattern of no amplification in TEC from infected animals (miR-144, miR-208b, miR-291b-3p, miR-295, miR-302a, miR-488, and miR-654-3p, Figure S4 in). [score:1]
[1 to 20 of 1 sentences]
65
[+] score: 1
Other miRNAs from this paper: hsa-let-7f-1, hsa-let-7f-2, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-32, mmu-mir-1a-1, mmu-mir-133a-1, mmu-mir-134, mmu-mir-135a-1, mmu-mir-144, mmu-mir-181a-2, mmu-mir-24-1, mmu-mir-200b, mmu-mir-206, hsa-mir-208a, mmu-mir-122, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-181a-1, hsa-mir-214, hsa-mir-200b, mmu-mir-299a, mmu-mir-302a, hsa-mir-1-2, hsa-mir-122, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-144, hsa-mir-134, hsa-mir-206, mmu-mir-200a, mmu-mir-208a, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-24-2, mmu-mir-328, hsa-mir-200c, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-181b-2, mmu-mir-25, mmu-mir-32, mmu-mir-200c, mmu-mir-181a-1, mmu-mir-214, mmu-mir-135a-2, mmu-mir-181b-1, mmu-mir-181c, hsa-mir-200a, hsa-mir-302a, hsa-mir-299, hsa-mir-361, mmu-mir-361, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-367, hsa-mir-377, mmu-mir-377, hsa-mir-328, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-181b-2, hsa-mir-20b, hsa-mir-429, mmu-mir-429, hsa-mir-483, hsa-mir-486-1, hsa-mir-181d, mmu-mir-483, mmu-mir-486a, mmu-mir-367, mmu-mir-20b, hsa-mir-568, hsa-mir-656, mmu-mir-302b, mmu-mir-302c, mmu-mir-302d, mmu-mir-744, mmu-mir-181d, mmu-mir-568, hsa-mir-892a, hsa-mir-892b, hsa-mir-744, hsa-mir-208b, mmu-mir-1b, hsa-mir-302e, hsa-mir-302f, hsa-mir-1307, eca-mir-208a, eca-mir-208b, eca-mir-200a, eca-mir-200b, eca-mir-302a, eca-mir-302b, eca-mir-302c, eca-mir-302d, eca-mir-367, eca-mir-429, eca-mir-328, eca-mir-214, eca-mir-200c, eca-mir-24-1, eca-mir-1-1, eca-mir-122, eca-mir-133a, eca-mir-144, eca-mir-25, eca-mir-135a, eca-mir-568, eca-mir-133b, eca-mir-206-2, eca-mir-1-2, eca-let-7f, eca-mir-24-2, eca-mir-134, eca-mir-299, eca-mir-377, eca-mir-656, eca-mir-181a, eca-mir-181b, eca-mir-32, eca-mir-486, eca-mir-181a-2, eca-mir-20b, eca-mir-361, mmu-mir-486b, mmu-mir-299b, hsa-mir-892c, hsa-mir-486-2, eca-mir-9021, eca-mir-1307, eca-mir-744, eca-mir-483, eca-mir-1379, eca-mir-7177b, eca-mir-8908j
For instance, miR-208, miR-302 (a-d), miR-367 were not detected (at >10 cpm on average) in the heart tissue; miR-134 and miR-208a were not detected in skeletal muscles; miR-483 in liver; or miR-483 and miR-377 in bone [36]. [score:1]
[1 to 20 of 1 sentences]
66
[+] score: 1
miRNAs that showed high variance between samples in the microarray show strong consistency between microarray and qPCR (mmu-miR-208b-3p, mmu-miR-3473a, mmu-miR-709). [score:1]
[1 to 20 of 1 sentences]
67
[+] score: 1
Ji X Plasma miR-208 as a Biomarker of Myocardial InjuryClin. [score:1]
[1 to 20 of 1 sentences]
68
[+] score: 1
Other miRNAs from this paper: hsa-mir-208a, mmu-mir-208a, hsa-mir-208b
A miR-208-Mef2 axis drives the decompensation of right ventricular function in pulmonary hypertension. [score:1]
[1 to 20 of 1 sentences]
69
[+] score: 1
cortex, we found a single microRNA, Mirlet7f-1, with significant difference in association with Q, opposite sign of association with Q in striatum and cortex, and FDR<0.05 for association with Q in both tissues, and additional 6 microRNAs (Mir206, Mir301b, Mir92b, Mir378b, Mir208b, Mir449a) satisfying p<0.05 for association with Q in both tissues. [score:1]
[1 to 20 of 1 sentences]
70
[+] score: 1
In agreement with prior studies in animal mo dels of heart failure it was found that miR-21 and miR-208b increased both in the infarct area and in the border zone, miR-1 and miR-208a decreased in the infarct area, miR-133a decreased in the border zone whereas the trend decrease in the infarct area did not achieve statistical significance, and miR-133b exhibited only a non-significant diminution both in the infarct and in the border zone [18]– [22] (Figure S5). [score:1]
[1 to 20 of 1 sentences]