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114 publications mentioning hsa-mir-208a (showing top 100)

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

1
[+] score: 331
Other miRNAs from this paper: hsa-mir-208b
Ectopic expression of miR-208 led to downregulation of SOX6 protein, which resulted in the downregulation of p21, upregulation of cyclin D1 and phosphorylation of Rb. [score:12]
Overexpression of miR-208 promotes the proliferation and tumorigenicity of ESCC cells, probably through post-translationally downregulating SOX6 expression by targeting its mRNA 3′- UTR. [score:12]
All the results suggested that further silencing SOX6 expression in Kyse30-miR-208 -inhibitor and Kyse410-miR-208 -inhibitor cells could reverse the inhibitory effect of the miR-208 inhibitor on ESCC cells proliferation. [score:11]
In contrast, the expression level of p21 was upregulated, Cyclin D1 was downregulated, and Rb phosphorylation was decreased in cells transfected with the miR-208 inhibitor (Figure  4E). [score:11]
Moreover, the expression level of the p21 protein was downregulated, Cyclin D1 was upregulated, and phosphorylated Rb was increased in miR-208 overexpressing cells compared with the negative control cells. [score:10]
In our study, downregulation of SOX6 by miR-208 led to downregulation of p21, upregulation of cyclin D1, and induced phosphorylation of Rb, resulting in the promotion of cell proliferation and cell cycle progression. [score:10]
The anchorage-independent growth assay revealed that both Kyse30-miR-208 -inhibitor and Kyse410-miR-208 -inhibitor cells formed fewer and smaller-sized colonies than their corresponding negative control cells, indicating the inhibitory function of miR-208 inhibitor on ESCC tumorigenicity (Figure  3D). [score:8]
In the current study, we found that miR-208 negatively regulated SOX6 expression by targeting SOX6 3′ untranslated region (3′-UTR) in the sequence-specific manner. [score:8]
The negative regulation of SOX6 by miR-208 leads to upregulation of p21, downregulation of cyclinD1, and Rb phosphorylation. [score:8]
Meanwhile, we observed that the mRNA of the SOX6 downstream gene, p21 was significantly downregulated, and that of Cyclin D1 was significantly upregulated, by miR-208 (Figure  4D). [score:7]
It has also been reported that miR-208 downregulates the Ets1 proto-oncogene, which is closely involved in the regulation of cell proliferation, differentiation, metastasis, apoptosis, and angiogenesis, by targeting the Ets1 mRNA 3′-UTR [29]. [score:7]
B. The expression levels of SOX6 protein in Kyse30 and Kyse410 cells overexpressing or suppressing miR-208, by western blotting 48 hours after transfection. [score:7]
As predicted, western blotting analysis revealed that SOX6 expression decreased in the Kyse30 and Kyse410 ESCC cells ectopic expressing miR-208 and increased in cells suppressing miR-208 (Figure  4B). [score:7]
The results of the luciferase reporter assay showed that overexpression of miR-208 decreased, and suppression of miR-208 increased, the luciferase activity of the SOX6 3′-UTR-luciferase reporter, whereas a miR-208 with mutated seed sequence failed to show an inhibitory effect on the luciferase activity (Figure  4C). [score:6]
These results suggested that downregulation of miR-208 could suppress the proliferation and tumorigenicity of ESCC cells. [score:6]
Using publicly available algorithms (TargetScan, Pictar, miRANDA), we found that SOX6 was a potential target of miR-208 (Figure  4A). [score:5]
A. Real-time PCR analysis of miR-208 expression in Kyse30 and Kyse410 cells transfected with miR-208 inhibitor. [score:5]
The average miR-208 expression was normalized using U6 expression. [score:5]
A. Real-time PCR analysis of miR-208 expression in Kyse30 and Kyse410 cells stably expressing miR-208 and in control cells. [score:5]
These results suggest that miR-208 represents a potential onco-miR and participates in ESCC carcinogenesis by suppressing SOX6 expression. [score:5]
A. The expression levels of SOX6 in Kyse30-miR-208 -inhibitor and Kyse410-miR-208 -inhibitor cells that were transfected with SOX6-siRNA, as measured by western blotting. [score:5]
The expression of the miRNA was defined based on the threshold cycle (Ct), and relative expression levels were calculated as 2 [-[(Ct of miR-208) – (Ct of U6)]] after normalization with reference to expression of U6 small nuclear RNA. [score:5]
Overexpression of miR-208 in ESCC cells increased cell proliferation, tumorigenicity and cell cycle progression, whereas inhibition of miR-208 reduced cells proliferation, tumorigenicity and cell cycle progression. [score:5]
SOX6 is a direct target of miR-208 in ESCC cells. [score:4]
To examine whether miR-208 mediated-SOX6 downregulation was through the 3′-UTR of SOX6, the SOX6- 3′-UTR fragment, containing three miR-208 binding sites, was subcloned into a pGL3 luciferase reporter vector. [score:4]
For the first time, we have demonstrated that miR-208 expression is correlated with ESCC progression and might play an important role during ESCC development. [score:4]
All these results suggested that upregulation of miR-208 promoted the proliferation and tumorigenicity of ESCC cells. [score:4]
As shown in Figure  3A, B and C, suppression of miR-208 by transfection with the miR-208 inhibitor significantly decreased the growth rate of both ESCC cell lines as compared with that of NC transfected cells. [score:4]
In this study, we found that miR-208 is upregulated in ESCC cell lines and tissues. [score:4]
Collectively, these results suggested that miR-208 was upregulated in ESCC. [score:4]
The results reveal that miR-208 is upregulated in ESCC cell lines and tissues. [score:4]
Figure 2 Upregulation of miR-208 promotes the proliferation ability of ESCC cells. [score:4]
In the current study, we demonstrated that miR-208 is upregulated in ESCC cell lines and tissues. [score:4]
Additionally, flow cytometry showed a significant increase in the percentage of cells in G1/G0 phase and a decrease in the percentage of cells in S phase in Kyse30-miR-208 -inhibitor and Kyse410-miR-208 -inhibitor cells compared with NC transfected cells (Figure  3E). [score:4]
Additionally, SOX6 was identified as a direct target of miR-208. [score:4]
Figure 4 miR-208 directly targets the 3′-UTR of SOX6 mRNA. [score:4]
To investigate the effect of miR-208 on the development and progression of ESCC, Kyse30 and Kyse410 ESCC cells, which were with medium-level of miR-208 expression, stably overexpressing miR-208 were established (Figure  2A). [score:4]
Furthermore, our data indicated that SOX6 mRNA is a target of miR-208 and that SOX6 is essential for the regulation of miR-208 in ESCC cells in vitro. [score:4]
miR-208 was upregulated in ESCC cell lines and tissues. [score:4]
Additionally, we identified SOX6 mRNA as a direct and functional target of miR-208. [score:4]
A. Real-time PCR analysis of miR-208 expression in normal esophageal epithelial cells (NEEC) and esophageal squamous carcinoma cells, including Kyse140, Kyse30, Kyse510, Kyse520, Eca109, TE-1, Kyse410, Kyse180, EC18, HKESC1 and 108CA. [score:3]
The miR-208 expression plasmid was generated by cloning the genomic pre-miR-208 gene, with 300-bp on each flanking side, into retroviral transfer plasmid pMSCV-puro (Clontech Laboratories Inc. [score:3]
Finally, we revealed that SOX6 suppression is essential for miR-208 -induced cell proliferation in ESCC. [score:3]
Consistently, miR-208 with mutated seed sequence failed to show an inhibitory effect on the luciferase activity of SOX6. [score:3]
miR-208 expression is elevated in ESCC cell lines and tissues. [score:3]
A. Schematic representation of the miR-208 target sites in the 3′-UTR of SOX6 mRNA and a miR-208 mutant containing two altered nucleotides in the seed sequence (miR-208-mut). [score:3]
The miR-208 mimic, miR-208 inhibitor and negative control (NC) were purchased from RiboBio (RiboBio Co. [score:3]
Furthermore, miR-208 overexpression promotes cell proliferation and tumorigenicity in human ESCC cell lines in vitro. [score:3]
E. of indicated ESCC cells transfected with miR-208 -inhibitor or NC. [score:3]
Nevertheless, the expression level of miR-208 in esophageal cancer or other cancers and its clinical relevance, require further study. [score:3]
Inhibition of miR-208 reduces proliferation of ESCC cells. [score:3]
SOX6 suppression is critical for miR-208 -induced cell proliferation in ESCC. [score:3]
Figure 1 Expression of miR-208 is increased in ESCC cell lines and tissues. [score:3]
Figure 3 Inhibition of miR-208 reduces the proliferation of ESCC. [score:3]
Figure 5 miR-208 promotes ESCC progression by inhibiting SOX6. [score:3]
B. The expression of miR-208 was examined in 10 paired cancerous tissues (T) and their adjacent noncancerous esophageal tissues (ANT). [score:3]
Inhibition of miR-208 improved cardiac function and patient survival during heart failure [27, 28]. [score:3]
However, the expression and function of miR-208 in cancers remain unknown. [score:3]
These data confirmed that miR-208 promoted ESCC cells proliferation and tumorigenicity by repressing endogenous SOX6 expression and that SOX6 plays important role in miR-208 -mediated cell proliferation. [score:3]
These data suggested that overexpression of miR-208 favored ESCC progression. [score:3]
Ectopic expression of miR-208 enhances proliferation of ESCC cells. [score:3]
The expression of miR-208 was examined in ESCC cell lines and tumor tissues by real-time PCR. [score:3]
Collectively, our results suggested that SOX6 was a bona fide target of miR-208. [score:3]
In summary, we describe, for the first time, that miR-208 plays an important role in ESCC development and progression. [score:2]
Real-time PCR analysis revealed that miR-208 expression was markedly increased in all eleven ESCC cell lines, including Kyse140, Kyse30, Kyse510, Kyse520, Eca109, TE-1, Kyse410, Kyse180, EC18, HKESC1 and 108CA, compared with that in NEEC (Figure  1A). [score:2]
The target of miR-208 was determined by western blotting analysis, luciferase reporter assay and real-time PCR. [score:2]
We verified a functional role for miR-208 in ESCC cell proliferation, tumorigenicity and cell cycle regulation. [score:2]
Moreover, comparative analysis revealed that miR-208 was significantly overexpressed in 10 pairs of cancerous tissues compared with the adjacent noncancerous esophageal tissues (Figure  1B). [score:2]
We demonstrated that miR-208 might play essential role via the SOX6 -mediated pathway during ESCC progression. [score:1]
miR-208 has been identified as a myomiR. [score:1]
, Moutain View, CA, USA) to generate plasmid pMSCV-miR-208. [score:1]
Further study is required to identify the clinical relevance and utility of miR-208 in ESCC diagnosis and therapy. [score:1]
The MTT and colony formation assays showed that overexpression of miR-208 dramatically increased the growth rate of both ESCC cell lines compared with that of control cells (Figure  2B and C). [score:1]
The MTT assay and the colony formation assay both showed that silencing SOX6 in miR-208 inhibitor transfected cells increased the growth rate of the cells (Figure  5B and C). [score:1]
To further test whether endogenous miR-208 helps to sustain the proliferative property of ESCC cells, loss-of-function studies using a miR-208 inhibitor were used to further investigate whether endogenous miR-208 helps to maintain the proliferative properties of ESCC cells. [score:1]
E. Effects of miR-208 overexpression on the cell cycle progression of ESCC cells measured by flow cytometry analysis. [score:1]
Proliferation capability of ESCC cells upon regulation of miR-208 expression was detected by MTT assay, colony formation assay, anchorage-independent growth ability assay and flow cytometry analysis. [score:1]
Based on these results, we propose that miR-208 might be used as a therapeutic agent for ESCC. [score:1]
pMSCV-miR-208 or pMSCV-NC was cotransfected with the PIK packaging plasmid into 293FT cells using the standard calcium phosphate transfection method [18]. [score:1]
Moreover, we analyzed the cell cycle of Kyse30-miR-208 and Kyse410-miR-208 cells by flow cytometry, which showed a significant decrease in the percentage of cells in G1/G0 phase and an increase in the percentage of cells in S phase (Figure  2E). [score:1]
Our results suggest that miR-208 may promote cell proliferation, tumorigenicity and cell cycle progression in ESCC through the SOX6 -mediated signaling pathway. [score:1]
Whether miR-208 is involved in SOX6 -associated LN metastasis needs further study. [score:1]
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By knocking down or overexpressing miR-208a-3p in gastric cancer cells, we validated that miR-208a-3p directly inhibited PDCD4 translation. [score:9]
MKN45 cells were infected with a control lentivirus or a lentivirus to overexpress miR-208a-3p, or transfected with a PDCD4 overexpression plasmid, or co -transfected with a miR-208a-3p overexpression lentivirus and a PDCD4 overexpression plasmid. [score:9]
MKN45 cells were infected with a control lentivirus or a miR-208a-3p overexpression lentivirus, or transfected with a PDCD4 overexpression plasmid, or co -transfected with a miR-208a-3p overexpression lentivirus and a PDCD4 overexpression plasmid. [score:9]
In this study, we identified PDCD4 as a direct target gene of miR-208a-3p and showed that miR-208a-3p inhibited PDCD4 expression directly. [score:9]
Next, MKN45 cells were infected with a control lentivirus or the miR-208a-3p overexpression lentivirus, or transfected with the PDCD4 overexpression plasmid, or co -transfected with the miR-208a-3p overexpression lentivirus and PDCD4 overexpression plasmid, and then the infected or transfected cells were subcutaneously injected into SCID mice. [score:9]
Xenografts with both miR-208a-3p and PDCD4 overexpression exhibited promoted cell apoptosis compared to xenografts with miR-208a-3p overexpression (Figure 5H), suggesting that PDCD4 overexpression could attenuate the suppressive effect of miR-208a-3p on cell apoptosis. [score:8]
Tumors with both miR-208a-3p and PDCD4 overexpression exhibited significantly higher levels of PDCD4 compared to tumors with miR-208a-3p overexpression (Figures 5F and 5G), suggesting that PDCD4 overexpression could rescue the PDCD4 suppression caused by miR-208a-3p. [score:8]
To overexpress PDCD4, an expression plasmid designed to specifically express the full-length ORF of PDCD4 without the miR-208a-3p-responsive 3′-UTR was constructed and transfected into MKN45 cells. [score:7]
The results revealed that miR-208a-3p inhibited PDCD4 expression and consequently suppress cell apoptosis, both in vitro and in vivo. [score:7]
Because miRNAs are generally thought to have expression patterns that are opposite to that of their targets [12, 13], we investigated whether miR-208a-3p expression was inversely correlated with PDCD4 expression in gastric cancer. [score:7]
We also provided evidence that restoration of PDCD4 expression can reverse miR-208a-3p -suppressed cell apoptosis, suggesting that the targeting of PDCD4 is one mechanism by which the miR-208a-3p exerts its tumorigenesis function. [score:7]
Consequently, the expression of the PDCD4 protein was distinctly reduced by the overexpression of miR-208a-3p and increased by the knockdown of miR-208a-3p in MKN45, HGC-27 and AGS cells (Figure 3B and 3C). [score:6]
Knockdown of miR-208a-3p was achieved by transfecting a miRNA inhibitor (a chemically modified single-stranded antisense oligonucleotide designed to specifically target the mature miRNA). [score:6]
Taken together, our results indicate that miR-208a-3p directly recognizes and binds to the 3′-UTR of the PDCD4 transcript and inhibits PDCD4 translation. [score:6]
Figure 4(A) The apoptosis assay was performed 24 h after the transfection of MKN45 cells with equal doses of the pre-miR-208a-3p, anti-miR-208a-3p or scrambled negative control RNAs (upper panel), or with equal doses of control siRNA, PDCD4 siRNA, control plasmid or PDCD4 overexpression plasmid (middle panel), or with equal doses of pre-miR-control plus control plasmid, pre-miR-control plus PDCD4 overexpression plasmid, pre-miR-208a-3p plus control plasmid, or pre-miR-208a-3p plus PDCD4 overexpression plasmid (lower panel). [score:6]
To clarify the regulatory level at which miR-208a-3p influenced PDCD4 expression, we repeated the above experiments and examined the expression of PDCD4 mRNA after transfection. [score:6]
Regulation of PDCD4 by miR-208a-3p may explain why the upregulation of miR-208a-3p during carcinogenesis can promote cancer progression. [score:5]
miR-208a-3p suppresses apoptosis of gastric cancer cells by targeting PDCD4. [score:5]
Similarly, PDCD4 overexpression attenuated the promotive effect of tumor growth caused by miR-208a-3p overexpression (Figure 5H and 5J). [score:5]
We first generated a viral expression construct to express miR-208a-3p. [score:5]
Therefore, we searched for miRNAs that could target PDCD4 and experimentally validated PDCD4 as a target of miR-208a-3p. [score:5]
When MKN45 cells were simultaneously transfected with pre-miR-208a-3p and the PDCD4 overexpression plasmid, PDCD4 dramatically rescued the suppressive effect of miR-208a-3p on cell apoptosis (Figure 4A and 4B). [score:5]
A 300-bp fragment containing the genomic miR-208a-3p sequence was cloned into a lentiviral expression vector, and MKN45 cells were infected with the lentivirus to overexpress miR-208a-3p. [score:5]
Immunohistochemical staining also revealed the presence of lower levels of PDCD4 in the tumors from mice implanted with miR-208a-3p -overexpressing cells, whereas the tumors from the PDCD4 -overexpressing mice showed increased PDCD4 protein levels (Figure 5H and 5I). [score:5]
PDCD4 is a direct target of miR-208a-3p. [score:4]
We observed a significant increase in the size and weight of the tumors in the miR-208a-3p -overexpressing group compared to the control group, whereas the size and weight of the tumors in the group implanted with the PDCD4-overexpression plasmid were dramatically decreased (Figure 5B and 5C). [score:4]
Therefore, modulation of PDCD4 by miR-208a-3p and miR-21 might explain, at least in part, why the upregulation of miR-208a-3p and miR-21 during tumorigenesis can silence PDCD4 and promote tumor cell growth and gastric cancer formation. [score:4]
Tumors from the miR-208a-3p -overexpressing group displayed reduced PDCD4 protein levels compared to tumors from the control group, whereas the PDCD4 -overexpressing group showed elevated PDCD4 protein levels (Figure 5F and 5G). [score:4]
Overexpression or knockdown of miR-208a-3p. [score:4]
The correlation between miR-208a-3p and PDCD4 was examined by evaluating PDCD4 expression in human gastric cancer cell lines (MKN45, HGC-27 and AGS) after overexpression or knockdown of miR-208a-3p. [score:4]
Validation of PDCD4 as a direct target of miR-208a-3p. [score:4]
The previous studies indicate that miR-208-3p is dysregulated in some cardiovascular and muscular diseases [16– 18]. [score:4]
These results demonstrated that miR-208a-3p specifically regulate PDCD4 expression at the post-transcriptional level. [score:4]
Luciferase activity of the mutated luciferase reporter was unaffected by either the overexpression or knockdown of miR-208a-3p (Figure 3E), suggesting that the binding sites strongly contribute to the miRNA:mRNA interaction. [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]
Thus, PDCD4 was regarded as a miR-208a-3p target based on both computational predictions and the inverse correlation between miR-208a-3p levels and PDCD4 protein levels in human gastric cancer. [score:3]
A mammalian expression plasmid encoding the full-length human PDCD4 open reading frame without the miR-208a-3p-responsive 3′-UTR was purchased from Invitrogen. [score:3]
Synthetic mimic (pre-miR-208a-3p), inhibitor (anti-miR-208a-3p) and scrambled negative control RNA (pre-miR-control and anti-miR-control) were purchased from RiboBio (Guangzhou, China). [score:3]
Additionally, PDCD4 overexpression attenuated the promotive effect of miR-208a-3p on tumor growth (Figure 5B and 5C), suggesting that miR-208a-3p might promote tumor growth by silencing PDCD4. [score:3]
The predicted interaction between miR-208a-3p and the targeting sites within the PDCD4 3′-UTR is illustrated in Figure 2A. [score:3]
Identification of conserved miR-208a-3p target sites within the 3′-UTR of PDCD4. [score:3]
For miRNA overexpression, equal amounts of pre-miR-208a-3p or pre-miR-control were used in each well. [score:3]
miR-208 is wi dely known to play a critical role in the formation of cardiovascular and muscular diseases [16– 18]. [score:3]
Twenty-four hours after transfection with pre-miR-208a-3p, anti-miR-208a-3p, PDCD4 siRNA and the overexpression plasmid, MKN45 cells were treated with RPMI 1640 medium with 2% FBS containing TRAIL(20ng/ml) for 24 h to induce apoptosis. [score:3]
A sequence containing the presumed miR-208a-3p binding site was designed from the human PDCD4 3′-untranslated region (3′-UTR). [score:3]
As expected, luciferase reporter activity was reduced to 40% in cells transfected with pre-miR-208a-3p, whereas inhibition of miR-208a-3p resulted in a two-fold increase in reporter activity (Figure 3E). [score:3]
The expression of mature miR-208a-3p was found to be 4-fold higher than the endogenous miRNA levels (Supplementary Figure S4). [score:3]
These results reveal that PDCD4 is crucial for the apoptosis of gastric cancer cells and that miR-208a-3p is able to suppress cell apoptosis by silencing PDCD4. [score:3]
In addition, we showed that the cellular phenotypes especially cell apoptosis was regulated by miR-208a-3p via negatively regulating PDCD4. [score:3]
Consequently, miR-208a-3p suppressed the apoptosis of gastric cancer cells in vitro and accelerated gastric tumor growth in vivo. [score:3]
As shown in Figure 4C and 4D, the activation of caspase-3 significantly decreased in cells transfected with pre-miR-208a-3p and the PDCD4 siRNA, but increased in cells transfected with anti-miR-208a-3p and the PDCD4 overexpression plasmid (Figure 4C and 4D). [score:3]
We also extracted total RNA and protein from each xenograft and analyzed miR-208a-3p and PDCD4 expression. [score:3]
Overexpression of miR-208a-3p was achieved by transfecting gastric cancer cells with a miRNA mimic (a synthetic RNA oligonucleotide duplex mimicking the miRNA precursor). [score:3]
Figure 3(A) Quantitative RT-PCR analysis of the expression levels of miR-208a-3p in MKN45, HGC-27 and AGS cells transfected with equal doses of the pre-miR-208a-3p, anti-miR-208a-3p or scrambled negative control RNAs (pre-miR-control or anti-miR-control). [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]
These results were consistent with the findings of the in vitro assays, which firmly validated the oncomiR role of miR-208a-3p in tumorigenesis through the targeting of PDCD4. [score:2]
Among the candidate miRNAs, miR-208a-3p was predicted to be a PDCD4 regulator by all three algorithms and was selected for further experimental verification. [score:2]
Furthermore, Hematoxylin and eosin (H&E) staining of xenograft tissues showed more cell pathological mitosis in the group implanted with the miR-208a-3p lentivirus compared with the control group, whereas confluent necrotic areas and more apoptotic cells were observed in the xenografts from the PDCD4 -overexpressing group (Figure 5H). [score:2]
Next, we engineered a mutant plasmid by introducing point mutations into the corresponding complementary seed site in the PDCD4 3′-UTR to eliminate the predicted miR-208a-3p binding sites. [score:2]
For the luciferase reporter assays, AGS cells were cultured in 24-well plates, and each well was transfected with 0.4 μg of firefly luciferase reporter plasmid, 0.4 μg of a β-galactosidase (β-gal) expression plasmid (Ambion), and equal amounts (20 pmol) of pre-miR-208a-3p, anti-miR-208a-3p, or the scrambled negative control RNAs using Lipofectamine 2000 (Invitrogen). [score:2]
The results generalized a novel regulatory network employing miR-208a-3p and PDCD4 to fine-tune cell apoptosis. [score:2]
Next, we focused on studying the role of miR-208a-3p in regulating PDCD4. [score:2]
Tumors from the miR-208a-3p-overexpression group showed a significant increase in the miR-208a-3p levels compared to tumors from the control group (Figure 5D). [score:2]
To investigate whether miR-208a-3p regulates PDCD4 expression through binding to the 3′-UTR of PDCD4 mRNA, the entire 3′-UTR of PDCD4 mRNA containing the presumed miR-208a-3p binding sites was fused downstream of the firefly luciferase gene in a reporter plasmid. [score:2]
For miRNA knockdown, equal amounts of anti-miR-208a-3p or anti-miR-control were used. [score:2]
We investigated whether the overexpression or knockdown of miR-208a-3p or PDCD4 would affect cell apoptosis in MKN45 cells induced by TRAIL using flow cytometry analysis. [score:2]
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]
Figure 2(A) Schematic description of the hypothetical duplexes formed by the interactions between the binding sites in the PDCD4 3′-UTR (top) and miR-208a-3p (bottom). [score:1]
Prediction of the miR-208a-3p binding site within the PDCD4 3′-UTR. [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]
Effect of miR-208a-3p and PDCD4 on the apoptosis of gastric cancer cells. [score:1]
The influence of miR-208a-3p and PDCD4 on the growth of gastric cancer cells in vivo. [score:1]
To test the binding specificity, the sequences that interacted with the seed sequence of miR-208a-3p were mutated (from GUCUUAA to CAGAAUU), and the mutant PDCD4 3′-UTR was inserted into an equivalent luciferase reporter. [score:1]
Firefly luciferase reporters containing either wild-type (WT) or mutant (MUT) miR-208a-3p binding sites in the PDCD4 3′-UTR were co -transfected into AGS cells with equal doses of the pre-miR-208a-3p, anti-miR-208a-3p or scrambled negative control RNAs. [score:1]
In summary, this study not only reveals a critical role for miR-208a-3p as an oncogenic miRNA in gastric carcinogenesis but also explores the molecular mechanisms by which miR-208a-3p contributes to gastric cancer progression. [score:1]
In this study, we detected an inverse correlation between miR-208a-3p levels and PDCD4 protein levels in human gastric cancer tissues and paired noncancerous tissues. [score:1]
As shown in this figure, the 3′-UTR of PDCD4 contained two conserved binding sites for miR-208a-3p. [score:1]
Detection of an inverse correlation between miR-208a-3p and PDCD4 levels in gastric cancer tissues. [score:1]
After measuring the expression levels of miR-208a-3p in the same 16 pairs of gastric cancer tissues and matched noncancerous tissues, we identified that the miR-208a-3p levels were remarkably higher in the cancer tissues (Figure 2B). [score:1]
The resulting plasmid was transfected into AGS cells along with pre-miR-208a-3p, anti-miR-208a-3p or scrambled negative control RNAs. [score:1]
Effects of miR-208a-3p and PDCD4 on the growth of gastric cancer cell xenografts in mice. [score:1]
Thus, miR-208a-3p and PDCD4 exerted opposing effects on cell apoptosis. [score:1]
One such example is miR-208. [score:1]
But in gastric cancer, the expression profile of miR-208a-3p has not been systematically investigated and the precise function of this miRNA in gastric tumorigenesis remains to be elucidated. [score:1]
The cell proliferation rate was decreased in the group implanted with the PDCD4 plasmid and increased in the group implanted with the miR-208a-3p lentivirus (Figure 5H and 5J). [score:1]
Cellular miR-208a-3p levels were significantly increased in MKN45, HGC-27 and AGS cells when these cells were transfected with pre-miR-208a-3p, and miR-208a-3p levels were decreased when these cells were transfected with anti-miR-208a-3p (Figure 3A). [score:1]
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showed that miR-208a mimics down-regulated the expression of apoptotic protein PARP1 and Bax and up-regulated the anti-apoptotic protein Bcl-2 in A549 cells (Fig.   4c). [score:9]
Forced expression of miR-208a promoted cell proliferation and induced radioresistance via targeting p21 with a corresponding activation of the AKT/mTOR pathway in lung cancer cells, whereas down-regulation of miR-208a resulted in the opposite effects. [score:8]
Our report also showed that up-regulation of miR-208a decreased the percentage of cells undergoing apoptosis and promoted G1 phase arrest, while inhibition of miR-208a in H1975 cells, which over-expressed this miRNA, results in the opposite effects. [score:8]
Nine miRNAs, including miR-29b-3p, miR-200a-3p, and miR-126-3p were significantly down-regulated, whereas miR-208a was the only miRNA that was up-regulated in the serum of the patients after radiation treatment (P < 0.05). [score:7]
As shown in Additional file 4: Figure S2A and S2B, the mimics enhanced the miR-208a expression in the two cell lines, and the inhibitor caused a significant decrease of miR-208a expression (P < 0.05). [score:7]
As shown in Figs.   3a and b, over -expression of miR-208a increased the proliferation rate, and the cells transiently transfected with the miR-208a mimics exhibited higher clonogenic survival rates than cells transfected with miRNA-NC, whereas down-regulation of miR-208a caused the opposite effect (Fig.   3c, P < 0.05). [score:6]
In addition, down-regulation of miR-208a increased the percentage of cells undergoing apoptosis and inhibited the G1 phase arrest in NSCLC cells. [score:6]
Western blot assays showed that the level of p21 protein was reduced significantly by miR-208a over -expression, whereas miR-208a down-regulation promoted p21 expression while compared with control treatment (Fig.   2a). [score:6]
Conversely, promoting miR-208a expression increased the activity of the AKT/mTOR pathway, though it’s not significantly as the effect of the inhibitor (Fig.   2d). [score:5]
miR-208a expression was normalized to U6 expression. [score:5]
The qRT-PCR results showed that miR-208a was expressed in both NSCLC cell lines and non-cancerous bronchial epithelial cell lines, with clearly more pronounced expression in the H1975 cells (Fig.   1b). [score:5]
In contrast, the apoptosis rates in the miR-208a -overexpressing H1975 cells increased significantly after transfection with the miR-208a inhibitor (from 9.57 ± 0.47 % to 12.11 ± 0.76 %; Fig.   4b). [score:5]
Inhibition of miR-208a in the miR-208a -overexpressing H1975 cells produced the opposite effect (Fig.   4e and f). [score:5]
The miR-208a mimics and negative control miRNA (miRNA-NC) or miR-208a inhibitor and inhibitor-NC were all synthesized by GenePharma Co. [score:5]
Among the differentially expressed miRNAs, miR-208a promoted lung cancer cell proliferation and decreased cell apoptosis by targeting p21 and AKT/mTOR pathway. [score:5]
Alternatively, another recent report suggested that miR-208 is a potential onco-miRNA and participates in the carcinogenesis of esophageal squamous cells by suppressing SOX6 expression [32]. [score:5]
Relative miR-208a expression in A549 (A) and H1299 (B) cells following transfection with miR-208a mimics or inhibitors. [score:5]
A549 cells were transfected with the miR-208a mimics, negative control miRNA (miRNA-NC), miR-208a inhibitor or inhibitor-NC for 24 h before lysis. [score:5]
In H1975 cells, the apoptotic relative protein increased expression significantly after transfection with the miR-208a inhibitor (Fig.   4d), which was consistent with the results of flow cytometric analysis. [score:5]
To explore the mechanism by which miR-208a executes its function in lung cancer, we first analyzed its predicted target genes using three bioinformatic algorithms (TargetScan, PicTar and miRBase). [score:5]
Western blot analysis confirmed that transfection with the miR-208a inhibitor decreased the levels of p-AKT and p-mTOR expression when compared with the control group. [score:4]
These results indicated p21 as a target of miR-208a for its regulatory function in lung cancer. [score:4]
However, while we further examined cell apoptosis rate after combine treated with radiotherapy, down-regulation of miR-208a enhanced apoptosis rate after receiving 4 Gy of X-ray irradiation. [score:4]
In our study, we identified p21 is directly targeted by miR-208a, and correspondingly activated AKT and modulated its downstream effector mTOR in A549 cells, which was consistent with the results of Chen, et al. [42]. [score:4]
miR-208a directly targeted p21 and affected AKT/mTOR pathway. [score:4]
Taken together, these results showed that increased miR-208a expression promoted cell growth and colony formation. [score:3]
Previous studies have identified miR-208a as a potential therapeutic target for systemic metabolic disorders that affect the heart [33, 34]. [score:3]
The significantly altered miRNAs are listed in Table  1. We identified only one miRNA (miR-208a) that was up-regulated after radiotherapy in sera of the lung cancer patients compared with the same patients’ serum before radiotherapy. [score:3]
To illustrate the major source of miR-208a after radiotherapy, we detected miR-208a expression in the culture medium of A549 cells after 0 or 4Gy X-ray irradiation by qRT-PCR analysis. [score:3]
b qRT-PCR analysis of the expression of miR-208a in human lung cancer cell lines (A549, H1299, H1975 and H460) and non-cancerous bronchial epithelial cell lines (BEAS-2B and HBE). [score:3]
Validation of altered miR-208a expression upon radiotherapy in both lung cancer patient sera and human lung cancer cells. [score:3]
Over -expression of miR-208a promoted H1299 cell proliferation. [score:3]
Thus, miR-208a may serve as a potential therapeutic target for lung cancer patients. [score:3]
qRT-PCR validated the antagonistic effect of miR-208a mimics and miR-208a inhibitor in NSCLC cells. [score:3]
Moreover, we found that the expression of miR-208a in A549 and H1299 cells could be further induced by X-ray irradiation (Fig.   1c and d). [score:3]
However, whether miR-208a could serve as a potential diagnostic and therapeutic target in cancer merits needs further multi-central clinical studies. [score:3]
miR-208a mimics or inhibitor were each cotransfected with the above reporters into human lung cancer A549 cells. [score:3]
We further validated four representative differentially expressed miRNAs (miR-208a, miR-126-3p, miR-29b-3p and miR-200a-3p) as listed in Table  1 by qRT-PCR analysis. [score:3]
In contrast, transfection of pGL3-UTR-MUT, in which the putative binding site of miR-208a was mutated, showed no interference with activity after transfection with either miR-208a mimics or inhibitor (Fig.   2c). [score:3]
miR-208a, one of the mature products of miR-208, which is enriched in the heart, plays a crucial role in heart health and disease. [score:3]
Each of the plasmids and pRL-TK, were cotransfected into A549 cells, either with miR-208a mimics or inhibitor as indicated. [score:3]
The present study provides evidence that miR-208a can affect the proliferation and radiosensitivity of human lung cancer cells by targeting p21 and can be transported by exosomes. [score:3]
Our study demonstrated that radiotherapy produces multiple alterations in the miRNA expression profile in the serum of lung cancer patients and that miR-208a was notably increased in the serum after exposure to a total of 60 Gy X-ray irradiation. [score:3]
The expression of miR-208a could be induced by X-ray irradiation in lung cancer cells. [score:3]
f D [0], D [q] and calculated SER values of inhibitor-NC- and miR-208a inhibitor -transfected groups are shown. [score:3]
Fig. 3Over -expression of miR-208a promoted cellular proliferation. [score:3]
24 h after tranfection of miR-208a mimics or inhibitor, A549 cells were exposed to 0 or 4 Gy X-ray irradiation. [score:3]
The relative serum miR-208a expression level normalized to miR-16 and cellular miR-208a expression normalized to U6 were calculated using the equation described in the Materials and. [score:3]
The fold change of differentially expressed miRNAs (miR-29b-3p, miR-126-3p, miR-208a and miR-200a-3p) was determined for lung cancer patients after radiotherapy (AR) in comparison with before radiotherapy (BR). [score:3]
When the miR-208a inhibitor was transfected into the A549 cells, the cells exhibited smaller clonogenic survival rates after exposure to 8 Gy X-ray rradiation and became more sensitive to irradiation (SER = 1.17, Fig.   5d, e and f). [score:3]
a The average serum miR-208a expression in 30 paired serum samples from lung cancer patients before and after radiotherapy. [score:3]
The relative expression levels of miR-208a in (c) A549, (d) H1299 and (e) HBE cells after exposure to 0, 2, 4 or 8 Gy X-ray irradiation. [score:3]
Interestingly, our study showed that the expression of miR-208a could be induced by X-ray irradiation in lung cancer A549 and H1299 cells but not in the non-cancerous bronchial epithelial HBE cells, suggesting that lung cancer cells were likely to be the major source of increased miR-208a after radiotherapy. [score:3]
Small RNAs targeting miR-208a were transfected into A549 cells followed by irradiation with a range of X-ray doses. [score:3]
This led us to examine whether ectopic expression of miR-208a could reduce endogenous p21 protein levels in human lung cancer cell lines. [score:3]
Our findings suggest that miR-208a served as a novel tumor accelerator miRNA and may be a potential therapeutic target for the treatment of human lung cancer. [score:3]
Finally, to validate the antagonistic effect in NSCLC cells, the miR-208a mimics and miR-208a inhibitor were transfected into A549 and H1299 cells. [score:3]
As shown in Fig.   1a, miR-208a was significantly over-expressed in the AR groups compared with their corresponding BR groups with a P value of 0.039. [score:2]
The cells were transfected with 50 nM of either miR-208a mimics and miRNA-NC or miR-208a inhibitor and inhibitor-NC 24 h later and allowed to grow for another 48 h. The cell proliferation was measured using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2Htetrazolium bromide (MTT) assay 48 h after the transfection with the RNAs. [score:2]
Luciferase assay showed that miR-208a mimics repressed the activity of pGL3-UTR-WT remarkably, whereas transfection inhibitor enhanced the promoter activities (Fig.   2c). [score:2]
A luciferase reporter that contained the full-length 3′UTR of p21 (pGL3-UTR-WT) and the mutant reporter plasmid with mutation of the miR-208a binding site (pGL3-UTR-MUT) were constructed by Synbio Tech, Ltd. [score:2]
c Colony formation assays of A549 cells transfected with miR-208a mimics or miR-208a inhibitor. [score:2]
We further test the hypothesis that p21 be a target of miR-208a using luciferase assays. [score:2]
These results indicated that the AKT/mTOR signaling pathway is involved in the miR-208a -induced proliferation of human lung cancer cells. [score:1]
Serum exosome miR-208a was translocated into human lung cancer cells in an exosome -mediated manner. [score:1]
As shown in Fig.   5a, cells transfected with miR-208a mimics before exposure to 8 Gy X-ray irradiation exhibited higher clonogenic survival rates than those treated with radiation alone. [score:1]
miR-208a decreased cellular apoptosis and disturbed the cell cycle. [score:1]
Moreover, miR-208a from the serum exosome fraction of lung cancer patients could shuttle to A549 cells in a time -dependent manner, which was likely to contribute to the subsequent biological effects. [score:1]
The samples were derived from the same experiment and analyzed under the same experimental conditionsBecause the binding sites of miR-208a were predicted at positions 86-92 in the 3′-UTR of p21 mRNA (Fig.   2b). [score:1]
These results suggested that the p21/AKT/mTOR pathway was involved in the ability of miR-208a to increase the proliferation of human lung cancer cells. [score:1]
Studies have shown that miR-208 induces the epithelial to mesenchymal transition of pancreatic cancer cells and thereby promotes cell metastasis and invasion [31]. [score:1]
The results showed that the exosomes containing miR-208a could be incorporated into A549 cells in a time -dependent manner. [score:1]
These results suggested that miR-208a enhanced the radioresistance of the A549 lung cancer cells. [score:1]
We concluded that the source of radiation induced miR-208a was secreted from lung cancer cells. [score:1]
qRT-PCR analysis was performed to evaluate the miR-208a expression in this study. [score:1]
But transfection of miR-208a mimics did not show significant difference in our study (Additional file 6: Figure S4). [score:1]
The samples were derived from the same experiment and analyzed under the same experimental conditions Because the binding sites of miR-208a were predicted at positions 86-92 in the 3′-UTR of p21 mRNA (Fig.   2b). [score:1]
miR-208a modulated radiation -induced cell apoptosis. [score:1]
Our results showed that the exosomes isolated from the sera of lung cancer patients before or after radiotherapy contained miRNA-208a and were taken up by the recipient lung cancer cells. [score:1]
b Putative miR-208a binding sequences in the 3′-UTR of p21 mRNA. [score:1]
We further examined the biological function of miR-208a on cell viability, apoptotic death and cell cycle distribution in human lung cancer cells and explored the probable mechanism. [score:1]
Thus, for miR-208a, the qRT-PCR analysis confirmed the result obtained by microarray analysis, and the difference was even stronger (>2.178-fold) when validated in the 30 paired lung cancer serum samples than that was anticipated from the microarray studies. [score:1]
Subsequently, we focused our study on the biological function of the serum miR-208a and found that increased miR-208a played a role in a negative-feedback mechanism that promoted the proliferation and radioresistance of lung cancer cells. [score:1]
Taken together, these results revealed that miR-208a increased the proliferation of human lung cancer cells and decreased cellular apoptosis by modulating the cell cycle distribution in human lung cancer cells. [score:1]
In contrast, miR-208a could not be induced by X-ray irradiation in the non-cancerous bronchial epithelial HBE cells (Fig.   1e). [score:1]
The above results indicated that 3’UTR of p21 harbours a miR-208a binding site. [score:1]
miR-208a increased the radioresistance of A549 cells. [score:1]
b qRT-PCR analysis of miR-208a and miR-16 contained in the exosomes. [score:1]
miR-208a p21 Proliferation Radioresistance Serum exosomes Lung cancer Lung cancer has long been the most dangerous malignant tumor among males in both well developed and poorly developed countries and has surpassed breast cancer as the leading cause of cancer death among females in well developed countries [1]. [score:1]
c qRT-PCR analysis of miR-208a in culture medium of A549 cells. [score:1]
The miR-208a mimics enhanced the radioresistance of the A549 cells (SER = 0.92, Fig.   5b and c). [score:1]
showed that radiotherapy can induce miR-208a secretion from A549 cells to the culture medium (Fig.   6c). [score:1]
Then, the qRT-PCR results showed that miRNAs including miR-208a as well as the ubiquitous miR-16 were present in the purified exosomes (Fig.   6b). [score:1]
Our demonstration that miR-208a is present in exosomes supported the hypothesis that exosomes may be a vehicle by which to modulate recipient cell functions. [score:1]
miR-208a increased human lung cancer cell growth in vitro. [score:1]
We also found that irradiation increased miR-208a in the culture medium of A549 cells, which further supported this hypothesis. [score:1]
Our study expands the list of diverse functions of miR-208a in driving lung cancer proliferation and radiation response. [score:1]
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[+] score: 41
Efficacy studies in animal mo dels of heart disease using an LNA -modified targeting miR-208a indicated that subcutaneous delivery of-208a prevents disease-related cardiac remo deling, a decline in function, and death during diastolic heart disease (Montgomery et al, 2011). [score:9]
These findings imply that inhibition of miR-208, in addition to blocking cardiac remo deling in the setting of heart disease, can have profound effects on metabolism and imply that the heart plays an unexpected role in the regulation of systemic metabolism and energy expenditure based on a miR-208 -dependent mechanism. [score:6]
Although the expression level of miR-208a does not change significantly during cardiac stress, this miRNA appears to play a key role in the stress -induced induction of βMHC, the pathological counterpart of αMHC and is, thus, a relevant player during pathological remo deling that occurs during cardiac disease (van Rooij et al, 2007). [score:5]
Hence, additional studies in non-human primates will be important in pinpointing whether pharmacological inhibition of miR-208b in larger mammals induces comparable gene changes and biological effects as miR-208a inhibition does in rodents. [score:5]
These studies underscore the potential of -based therapies for modulating cardiac miRNAs and validate miR-208 as a therapeutic target for the modulation of cardiac function and remo deling during heart disease. [score:5]
Interestingly, myosin and subsequent miR-208 (myomiR) expression differs significantly between species. [score:3]
Inhibition of miR-208 for the treatment of heart failure and diabetes. [score:3]
While αMHC/miR-208a is the predominant cardiac myosin in rodents, expression of βMHC/miR-208b is more prevalent in larger mammals. [score:3]
Shortly after the first report on miR-208a, it was discovered that the βMHC gene also contains an intronic miR-208 isoform, named miR-208b (van Rooij et al, 2009). [score:1]
Several years ago, it was discovered that this gene not only gives rise to a key protein, but additionally produces a miRNA, known as miR-208a (van Rooij et al, 2007). [score:1]
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5
[+] score: 39
Given that translational up-regulation by miRNAs has also been observed as a result of the direct action of miRNAs (reviewed in Valinezhad Orang et al., 2014[158]; Vasudevan, 2012[160]), it is possible that miR-208a-5p binding to this predicted MRE results in the detected up-regulation of rat endoglin. [score:10]
Therefore, it is possible that the elevated endoglin levels could be the result of secondary regulatory events (i. e. down-regulation of a miR208a target that results in elevated endoglin expression). [score:9]
This same laboratory also established that miR-208a-5p and endoglin expression was up-regulated in an in vivo volume overload -induced heart failure rat mo del (Wang et al., 2014[165]) (Table 8 (Tab. [score:6]
Taken together it is clear that more studies are needed to determine the mechanism by which miR-208a-5p regulates rat endoglin gene expression and to investigate whether this mechanism is also employed in regulating human ENG gene expression. [score:5]
Shyu et al. (2013[147]) speculate that miR-208a-5p may interact with a MRE located in the promoter region of the rat Eng gene, which in turn induces rat endoglin gene expression. [score:3]
Shyu et al. (2013[147]) demonstrated that mechanical stretch and TGFβ1 increased miR-208a-5p and endoglin mRNA and protein expression in rat cardiac myoblasts (Table 8 (Tab. [score:3]
Unfortunately, the predicted rat Eng promoter MRE does not show significant complementarity to miR-208a-5p and does not follow seed sequence rules. [score:1]
8); References in Table 8: miR-5739: Yoo et al., 2011[173]; miR-6087: Yoo et al., 2012[174]; miR-208a-5p: Shyu et al., 2013[147]; miR-208a-5p: Wang et al., 2014[165]; miR-15 family: Tijsen et al., 2014[155]; miR-370-3p: Chen et al., 2014[30]). [score:1]
Additionally, mouse endoglin mRNAs harbor a miR-208a-5p MRE located within the 3′-UTR that was predicted by Diana-microT-CDS (0.517 miTG score). [score:1]
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[+] score: 32
T2DM increased miR-208a expression in both ZDF-male and ZDF-female hearts, resulting in ZDF-females having the highest expression. [score:5]
Notably, both miR-208a and Med13 expression levels were higher in ZL-female rats, indicating that in healthy female rats, other mechanisms contributed to increased expression of Med13; however, this advantage was lost in diabetic ZDF-female rats. [score:5]
However, in healthy female rats with intact ovary, cardiac miR-208a expression was higher than that seen in males, indicating that estrogen -mediated regulation of miR-208a in vivo is different. [score:4]
Notably, ex vivo studies on mouse aorta showed that miR-208a was suppressed by estrogen (Zhao J. et al., 2013). [score:3]
Med13 mRNA is an established target of miR-208a (Grueter et al., 2012; Gul et al., 2015). [score:3]
T2DM suppressed cardiac Med13 mRNA levels in both sexes, which is consistent with the T2DM -induced increase in miR-208a. [score:3]
Regulation of cardiac miR-208a, an inducer of obesity, by rapamycin and nebivolol. [score:2]
One of the molecules that regulates cardiac conduction and hypertrophy is the microRNA (miRNA) miR-208a (Callis et al., 2009). [score:2]
Interestingly, miR-208a exhibits sex differences, with expression being higher in the heart tissues of ZL-female rats compared to ZL-male rats (Lum-Naihe et al., 2017). [score:2]
Thus miR-208a is a miRNA that links T2DM and cardiac dysfunction and hypertrophy. [score:1]
Additionally, miR-208a and miR-29a/b/c are increased, while FA utilization, mitochondrial function, fibrosis, Agtr2-Med13 signaling, capillary density, collagen 1a, and NRP-1 are decreased (Widdop et al., 2003; Miki et al., 2013; Schilling and Mann, 2014; Lum-Naihe et al., 2017). [score:1]
MicroRNA-208a is a regulator of cardiac hypertrophy and conduction in mice. [score:1]
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[+] score: 29
Literature search and online target prediction tools (Target Scan and Pictar Scan) revealed miR-1 and miR-208a as possible inhibitors of Pim-1 expression [15, 17, 32]. [score:9]
This was associated with significant downregulation of pro-survival Pim-1 and upregulation of pro-apoptotic Caspase-3, microRNA-1 and microRNA-208a. [score:7]
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]
Here, we confirmed that female diabetic hearts more abundantly express miR-1 (Figure  3F) and miR-208a (Figure  3G) at 4 weeks after STZ -induced diabetes, with further increases during evolution of cardiomyopathy (P < 0.01 vs. [score:3]
C-D. Bar graphs showing the expression level of miR-1 (C) and miR-208a (D) in diabetic and non-diabetic human heart. [score:3]
Additional in vivo studies are necessary to understand the role of miR-1 and miR-208a in accelerating the development of cardiomyopathy in female diabetic hearts. [score:2]
In addition to miR-1, we also found early activation of miR-208a in the female diabetic mice, which might also account for increased LV dilation early in the female diabetic heart [42]. [score:1]
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]
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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-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-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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[+] score: 23
Of the differentially expressed miRNAs, miR-185, miR-150, miR-194, and miR-363 were downregulated in individuals with 22q11DS as compared to TD controls and miR-208, miR-190, and miR-1 were upregulated. [score:8]
In the presented study we observed an increased expression of miR-208 and miR-190 in 22q11DS compared to controls; interestingly a significant up-regulation of these miRNAs were reported in patients with myocardial infarction [69] suggesting their contributing role in cardiac disease. [score:7]
Muscle specific Dgcr8 [−/−] mice demonstrated downregulation of a subset of mature cardiac enriched miRNAs, specifically miR-1, miR-133a, and miR-208, and experienced premature lethality within 2 months likely due to cardiac failure [37]. [score:4]
Several miRNAs have been implicated in cardiogenesis and heart development including miR-1, miR208 and miR-190 [69]– [71]. [score:2]
We expected that some miRNAs, including miR-1 and miR-208, although differentially expressed in subjects with 22q11DS compared to TD, were dysregulated between individuals with 22q11DS with CHD compared to those without CHD, but we did not detect any difference in levels between the two groups. [score:2]
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[+] score: 22
Finally, the transcription factor est-1, which is yet another functionally validated miR-208a target, regulates many circadian genes in the SCN and is down-regulated during the day and upregulated during the night in rats [50]. [score:10]
miR-208a-3p (p = 0.003) has Sox-6 as one of its validated targets (as does miR-155-5p) and Sox-6 expression is negatively correlated with Per1 expression. [score:7]
Another miR-208a-3p target, CDKN1A (or p21), is a cyclin -dependent kinase inhibitor controlling G1 cell cycle progression and is circadian in a number of mouse tissues [41]. [score:5]
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11
[+] score: 22
miR-30b could be a potential biomarker of ACVIM stage B heart failure in Dachshunds and miR-133b could be a potential biomarker of ACVIM stage C. The lack of expression of miR-208a and 208b in healthy dogs and dogs with heart disease and lack of significant changes in expression in the remaining 5 miRNAs which are potential biomarkers of heart diseases in humans proves that the findings in human medicine are not always directly reflected in veterinary medicine. [score:10]
Although miR-208a and 208b are proposed as potential biomarkers of heart disease in humans [17, 28, 35] their expression has not been detected in any of the samples analyzed in our study. [score:5]
Likewise in ACVIM stage B class the expression of miR-208a and miR-208b were not detected (Figure  2). [score:3]
Expression of miR-208a and 208b was not detected. [score:3]
miR-208a and miR-208b were not detected in any of the examined samples (in both healthy group of dogs–ACVIM stage A and ACVIM stage B) (Figure  1). [score:1]
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12
[+] score: 22
The miRNA miR-208a downregulates CD14, CD40 ligand, PGI2 receptor, thromboxane A2 receptor, and programmed cell death (Recchiuti et al., 2011; Figure 8B), a tumor suppressor molecule that acts as a translational repressor of IL-10 (Sheedy et al., 2010), consistent with the existence of a seed region for miR-208a in the 3′ UTR of PDCD4. [score:8]
Quantitative PCR analysis of miRNAs isolated from peritoneal lavages collected 24 h post injection of zymosan showed that RvD1 significantly upregulated identified resolution miRs miR-208a and miR-219 in vivo (Recchiuti et al., 2011), whereas it does not appear to regulate miR-21, miR-146b, and miR-302d (Figure 9). [score:5]
In ALX/FPR2 [−/−] mice, RvD1 did not regulate PMN infiltration, consistent with recent results (Norling et al., 2012), nor did it significantly alter miR-208a or miR-219 expression at 24 h (Figure 9). [score:4]
RvD1-GPCR gene networks connecting target genes of miR-146b (A), miR-208a (B), and miR-219 (C). [score:3]
In these studies, miR-21, miR-146b, miR-208a, and miR-219 were significantly regulated at 12 and 24 h compared to 4 h (Figure 7), suggesting a role in resolution. [score:1]
RvD1, administered in its pro-drug carboxy methyl ester form, significantly lowered the Ψ [max] (from 15.0 to 11.5 × 10 [6]), and accelerated or shortened the R [i] by ∼4 h. Quantitative real-time PCR analyses carried out with exudates from zymosan- and zymosan plus RvD1 -treated mice revealed that RvD1 temporally controls the specific sets of pro-resolving miRNAs miR-21, miR-146b, miR-208a, and miR-219 (coined resolution miRs) in exudates in vivo. [score:1]
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[+] score: 21
Other miRNAs from this paper: hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-208b
MiR-208 have been reported to be a negative regulator of Mstn expression [32], and to be upregulated in various forms of cardiomyopathy [33, 34] and myocardial ischemia [35]. [score:6]
Heart failure Myostatin IGF-I Activin receptor IIB IGF-I receptor qRT-PCR microRNA-208 miRNA Myostatin (Mstn), the growth inhibitor of skeletal muscle [1], was shown to be expressed in the heart tissue [2] with controversial data about its role in myocardial physiology and pathophysiology. [score:5]
In paralell with these results miR-208 showed mild upregulation in the left ventricle of both DCM and ICM hearts. [score:4]
miR-208 expression in relation to Mstn expression in DCM and ICM patients compared to healthy controls. [score:4]
A comprehensive qRT-PCR analysis of Mstn and IGF-I signaling was carried out by measuring expression of Mstn, its receptor Activin receptor IIB (ActRIIB), IGF-I, IGF-I receptor (IGF-IR), and the negative regulator of Mstn miR-208, respectively. [score:2]
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[+] score: 20
There is an inter-regulation between these two forms, miR-208a promotes the upregulation of β-MHC and miR-208b and on the other hand, miR-208b promotes the downregulation of α-MHC and miR-208a (110). [score:8]
In humans, the ratio switch from fetal miR-208a to miR-208b expression occurs shortly after birth. [score:3]
Very interestingly, among the five candidates identified miR-208a was included. [score:1]
miR-208 is composed of miR-208a, a cardiac-specific miRNA which is embedded within an intron of the α-MHC gene and the related miR-208b, which is embedded within the β-MHC gene (109). [score:1]
The emerging role of miR-208a in the heart. [score:1]
Furthermore, it has brought to the forefront a specific set of miRNAs, namely, miR-1; miR-133; miR-208a/b, and miR-499a. [score:1]
Actually, this trans-differentiation has been achieved by Jayawardena et al. in 2015 using the exact same set of miRNAs that stood out in the above-mentioned studies on miRNAs as AMI biomarkers, namely miR-1, miR-133a, miR-208a, and miR-499a (104). [score:1]
Referring to the aforementioned multiple studies on miRNAs as AMI biomarker, a set of candidates has emerged: the four muscle-specific miRNAs, the myomiRs miR-1, miR-133, miR-208a/b, and miR-499a. [score:1]
Actually, miRNAs abundant in the myocardium, known as myomiRs, such as miR-1, miR-133, miR-208a/b, and miR-499a, were reported many times as being strongly increased in the serum or plasma of patients with AMI (36). [score:1]
miR-499, similarly to miR-208, is a mirtron located within an intron of a myosin heavy chain isoform gene, namely the gene Myh7b (109). [score:1]
The three myosin-related miRNAs, miR-208a/b, and miR-499, together control muscle myosin content, myofiber identity, and muscle performance. [score:1]
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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]
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]
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]
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Both over -expression and under -expression of miR-208a has been associated with cardiac arrhythmia [36], with apoptosis in ischemic cardiomyocytes [37] and generally with heart diseases [38]. [score:7]
Down-regulation of miR-208a in atrial myocardial tissues of patients with CHD after CPB underscore the integral function of this miRNA in regulating cell morphology and contractility. [score:5]
In particular, miR-208, a member of the miR-208 family, is differentially expressed during heart developmental and plays an essential role in normal cardiac conduction [34, 35]. [score:4]
MiRNAs known to be involved in myocardial development include miR-208a, miR-21, miR-145, miR-1, miR-133a and miR-29 [18– 20]. [score:2]
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17
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Also, transgenic over -expression of miR-208a in the heart was sufficient to induce hypertrophic growth in mice, which resulted in pronounced repression of the miR-208 regulatory target thyroid hormone -associated protein 1 and myostatin, two negative regulators of muscle growth and hypertrophy [56]. [score:7]
These studies indicate that miRNAs, miRNA-208, miRNA-23a, miRNA-24, miRNA-125, miRNA-21, miRNA-129, miRNA-195, miRNA-199, and miRNA-212 are frequently increased in response to cardiac hypertrophy, whereas, miRNA-29, miRNA-1, miRNA-30, miRNA-133, and miRNA-150 expression are often found to be decreased. [score:3]
Interestingly, suppression of miRNA-208a in heart failure rats prevents the pathological myosin switching while improving cardiac function [64]. [score:3]
Callis T. E. Pandya K. Seok H. Y. Tang R. H. Tatsuguchi M. Huang Z. P. Chen J. F. Deng Z. Gunn B. Shumate J. MicroRNA-208a is a regulator of cardiac hypertrophy and conduction in mice J. Clin. [score:1]
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[+] score: 14
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]
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]
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19
[+] score: 13
These data highlight the potential of antimiR -based approaches to pharmacologically inhibit cardiac miRNAs and strongly imply miR-208 as a therapeutic target for treatment of heart disease [102]. [score:7]
The miR-208a/b family and miR-499, designated as MyomiRs, are located in the introns of three myosin genes, Myh6, Myh7, and Myh7b, respectively, and play critical roles in the control of pathological cardiac hypertrophy, heart failure and myocardial infarction in humans and mouse mo dels of heart disease [10, 136]. [score:3]
Genetic deletion of miR-208 in mice showed no phenotype at baseline, whereas in response to cardiac stress, miR-208 knockout mice showed virtually no cardiomyocyte hypertrophy or fibrosis [137, 138]. [score:2]
Therapeutic silencing of miR-208a by subcutaneously (s. c. ) delivered LNA -modified antimiR-208a led to potent and sustained silencing of miR-208a in the rat heart. [score:1]
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[+] score: 12
In addition to miR-320a, we found a group miRNAs which are differentially expressed in CAD patients, among which miRNAs, miR-21, miR-30a, miR-126, and miR-133a were reported to be up-regulated and miR-208a and miR-320a to be downregulated in infarcted myocardium 35, 36. [score:9]
Seven miRNAs (miR-21, miR-30a, miR-126, miR-133a, miR-195, miR-208a and miR-320a) were confirmed to be differentially expressed between CAD and control samples (Fig. 1B). [score:3]
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Specifically, in these studies taken together, miR-1, miR-133a, miR-133b, miR-208, and miR-499 were found upregulated in plasma of AMI patients. [score:4]
Wang et al. [25] reported that, in AMI patients, miR-208 levels were not altered by chronic kidney disease or trauma, as it happens for troponins. [score:3]
More recently, in a systematic review [28] the authors proposed that only cardiomyocyte-enriched miRNAS, miR-1, miR-133a/b, miR-145, miR-208a/b, and miR-499(a) in plasma and/or serum are potential biomarkers for the diagnosis of coronary heart disease. [score:3]
Several miRNAs, as cardiomyocyte-enriched (miR-133, miR-208a) [41], endothelial cell-enriched (miR-126, miR-17-92a cluster), vascular smooth cell (miR-143/145) and inflammatory cell-enriched (miR-155), and platelet-enriched (miR-199a) miRNAs, were associated with CAD, while lipometabolism-related miR-122 and miR-370 increased as the severity of CAD quantified by the Gensini score increased [42]. [score:1]
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They induced TERT expression in the cultured neonatal rat cardiomyocytes via anoxia-reoxygenation mo deling and found the increased expression of immature (pri- and pre-) miR-1 and miR-29a, as well as mature miR-1. Conversely, siRNA -mediated TERT suppression decreased mature miR-21, miR-29a and miR-208a. [score:7]
Although they only focused on and tested miRNAs predominantly specific for the heart (miR-1, miR-21, miR-29a and miR-208a), their findings suggest that miRNA regulation by TERT may be a conserved gene regulatory mechanism across species. [score:3]
Drevytska T. I. Nagibin V. S. Gurianova V. L. Kedlyan V. R. Moibenko A. A. Dosenko V. E. Silencing of TERT decreases levels of miR-1, miR-21, miR-29a and miR-208a in cardiomyocytes Cell Biochem. [score:1]
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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-21, hsa-mir-22, hsa-mir-23a, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-33a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-96, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-16-2, hsa-mir-197, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-199a-2, hsa-mir-204, hsa-mir-210, hsa-mir-181a-1, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-mir-224, hsa-mir-200b, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-15b, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-130a, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-138-2, hsa-mir-140, hsa-mir-141, hsa-mir-142, hsa-mir-143, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-138-1, hsa-mir-146a, hsa-mir-193a, hsa-mir-194-1, hsa-mir-195, hsa-mir-206, hsa-mir-320a, hsa-mir-200c, hsa-mir-1-1, hsa-mir-155, hsa-mir-181b-2, hsa-mir-194-2, hsa-mir-106b, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-34b, hsa-mir-34c, hsa-mir-130b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-363, hsa-mir-365a, hsa-mir-365b, hsa-mir-369, hsa-mir-370, hsa-mir-371a, hsa-mir-375, hsa-mir-378a, hsa-mir-133b, hsa-mir-423, hsa-mir-448, hsa-mir-429, hsa-mir-486-1, hsa-mir-146b, hsa-mir-181d, hsa-mir-520c, hsa-mir-499a, hsa-mir-509-1, hsa-mir-532, hsa-mir-33b, hsa-mir-637, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, hsa-mir-378d-2, hsa-mir-509-2, hsa-mir-208b, hsa-mir-509-3, hsa-mir-103b-1, hsa-mir-103b-2, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, hsa-mir-378b, hsa-mir-320e, hsa-mir-378c, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-371b, hsa-mir-499b, hsa-mir-378j, hsa-mir-486-2
miR-206 is specifically expressed in the skeletal muscle, whereas miR-208a is cardio-specific; nevertheless, most of these miRNAs are co-expressed in the heart and skeletal muscles [110]. [score:5]
A fascinating research topic is the pleiotropic regulatory network exerted by miR-208a, a heart-specific miRNA that also controls glucose metabolism and energy homeostasis. [score:2]
The myomiRs include miR-1, miR-133a, miR-133b, miR-206, miR-208a, miR-208b, miR-486, and miR-499 [109]. [score:1]
For instance, miR-126 is reduced in T2D [148] and has been proposed as a biomarker of endothelial dysfunction caused by uncontrolled glycemia in T2D [149]; miR-1, miR-21, miR-133a, and miR-208 are enriched in the plasma after myocardial infarction [150]; miR-122 is enhanced in hepatic injury and steatosis [151], as well as let-7e in hypertension [152]. [score:1]
MED13 is negatively controlled by miR-208a. [score:1]
Remarkably, anti-miR-208 oligonucleotides confer resistance to diet -induced obesity and improve glucose tolerance in mice [120]. [score:1]
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[+] score: 11
Overexpression of miR-208 in prostate cancer cells prevented the inhibitory effects that CUR has on proliferation [193]. [score:5]
Furthermore, miR-208 specifically bound the 3′untranslated region (3′UTR) of CDKN1A mRNA. [score:3]
It was determined that miR-208 was specifically inhibited by CUR. [score:3]
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Of the three miRNAs present in less than 25% of high-risk women, miR-766-3p is down-regulated, while miR-4727-3p, and miR-208-5p are highly up-regulated. [score:7]
The mo dels generated the following risk score formulas: Formula 1: AUC-selected miRNA-mo deled risk score Risk score = (-1.062 x hsa-miR-3124-5p) + (-0.32 x hsa-miR-1184) + (-0.33 x hsa-miR-4423-3p) + (0.621 x hsa-miR-4529-3p) + (-0.626 x hsa-miR-7855-5p) + (0.359 x hsa-miR-4446-3p) Formula 2: ANOVA-selected miRNA-mo deled risk score Risk score = (-0.274 x hsa-miR-1184) + (-1.305 x hsa-miR-766-3p) + (-0.393 x hsa-miR-4423-3p) + (0.601 x hsa-miR-4727-3p) + (0.229 x hsa-miR-208a-5p) These formula-generated risk scores were applied to miRNA levels from each case and control for discriminatory power. [score:1]
The mo dels generated the following risk score formulas: Formula 1: AUC-selected miRNA-mo deled risk score Risk score = (-1.062 x hsa-miR-3124-5p) + (-0.32 x hsa-miR-1184) + (-0.33 x hsa-miR-4423-3p) + (0.621 x hsa-miR-4529-3p) + (-0.626 x hsa-miR-7855-5p) + (0.359 x hsa-miR-4446-3p) Formula 2: ANOVA-selected miRNA-mo deled risk score Risk score = (-0.274 x hsa-miR-1184) + (-1.305 x hsa-miR-766-3p) + (-0.393 x hsa-miR-4423-3p) + (0.601 x hsa-miR-4727-3p) + (0.229 x hsa-miR-208a-5p)These formula-generated risk scores were applied to miRNA levels from each case and control for discriminatory power. [score:1]
Of note, the 3 miRNAs unique to the ANOVA set (hsa-miR-766-3p, hsa-miR-4727-3p, and hsa-miR-208a-5p) were detected in less than 25% of patients (Table 2, Figure 4G-4I). [score:1]
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Based on the collected miRNA-circRNA interactions and the deregulated RNA molecules, we collected several abnormally expressed miRNAs, including 11 downregulated miRNAs (miR-124-3p, miR-129-5p, miR-135a-5p, miR-153-3p, miR-204-5p, miR-208a-3p, miR-211-5p, miR-218-5p, miR-488-3p, miR-490-3p, and miR-504-5p) and 1 upregulated miRNA (miR-373-3p). [score:10]
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Overexpression of miR-1 in infarcted myocardium can promote arrhythmogenesis, whereas arrhythmia could be alleviated through deleting endogenous miR-1. miR-208a, a cardiac-specific miRNA encoded by the intron of the myosin heavy chain gene Myh6, has also been demonstrated to play an important role in arrhythmogenesis [43], especially in the process of atrial depolarization, by regulating the expression of Connexin-40 (GJA5). [score:6]
Callis T. E. Pandya K. Seok H. Y. Tang R. H. Tatsuguchi M. Huang Z. P. Chen J. F. Deng Z. Gunn B. Shumate J. microRNA-208a is a regulator of cardiac hypertrophy and conduction in mice J. Clin. [score:2]
However, it was reported in a separated study that a combination of miR-1, miR-133, miR-208, and miR-499 was able to directly induce the cellular reprogramming of fibroblasts into cardiomyocyte-like cells in vitro [18]. [score:2]
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Although the expression level of miR-208 remains stable during cardiac stress, this miRNA appears to fulfill a dominant function in regulating cardiac hypertrophy and remo deling. [score:4]
MiR-208 is supposed to act by repressing the expression of a common component of stress-response and thyroid hormone signaling pathways in the heart, that of the thyroid-hormone-receptor (TR) co-regulator TR -associated protein 1 (THRAP1). [score:3]
MiR-208 is encoded within intron 27 of the α major histocompatibility complex (MHC) gene and plays a key role in the expression of β MHC in response to cardiac stress [20]. [score:2]
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miR-208 expression is associated with fibrosis and EMT progression as well as specifically targeting the BMP co-receptor, endoglin (Fig. 1) (Liu et al. 2014 a, Wang et al. 2014 a). [score:5]
Years of work on miRs in the cardiology field has revealed miR-208 to be elevated in cases of cardiac hypertrophy and heart failure (Callis et al. 2009, Montgomery et al. 2011, Oliveira-Carvalho & Bocchi 2016). [score:1]
If the clinical trial demonstrates miR-208 as a robust marker for cardiac damage, there will be a pre-clinical basis to consider the use of an antimiR-208 as a viable cardio-protective for chemotherapy patients (Callis et al. 2009, Montgomery et al. 2011, Tony et al. 2015). [score:1]
242606799) 12434020 Callis TE Pandya K Seok HY Tang RH Tatsuguchi M Huang ZP Chen JF Deng Z Gunn B Shumate J 2009 MicroRNA-208a is a regulator of cardiac hypertrophy and conduction in mice. [score:1]
2964) 22131135 Liu A Shao C Jin G Liu R Hao J Song B Ouyang L Hu X 2014a miR-208 -induced epithelial to mesenchymal transition of pancreatic cancer cells promotes cell metastasis and invasion. [score:1]
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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]
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Other miRNAs from this paper: hsa-mir-1-2, hsa-mir-1-1, hsa-mir-208b
mir-208 null mice do not hypertrophy in response to cardiac stress and null mice do not upregulate Myh7 [89, 90]. [score:4]
Silencing of miR-208 reduces cardiac remo deling, deterioration of heart function, and improves survival in a rat mo del of heart failure, while overexpression of miR-208 in cardiomyocytes leads to cardiomyocyte hypertrophy [90, 91]. [score:3]
For example, miR-208 is encoded by an intron within MYH6, which encodes α myosin heavy chain and is in close proximity to MYH7 [87, 88]. [score:1]
Callis T. E. Pandya K. Seok H. Y. Tang R. H. Tatsuguchi M. Huang Z. P. Chen J. F. Deng Z. Gunn B. Shumate J. MicroRNA-208a is a regulator of cardiac hypertrophy and conduction in mice J. Clin. [score:1]
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Other miRNAs from this paper: hsa-mir-208b
For instance, mir-208a, on an intron of MYH6, is a positive regulator of beta-MHC by targeting transcription factors that repress its expression [24]. [score:6]
GS scores for MYH6 and mir-208a accurately reflect their cardiac-specific expression, whereas MYH7 and mir-208b exhibit strong signals in both skeletal and cardiac tissue (Fig 3A and S5 Table). [score:3]
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While miR-208 is expressed only in the heart, mir-206 is skeletal muscle specific [35]. [score:3]
The analysis of miRNA expression in cardiomyocyte progenitor cells (CMPCs) showed that 188 miRNAs were detectable in proliferating CMPCs and 195 in differentiated CMPCs such as miR1, miR1-2, miR499, miR322, miR503, miR208, miR133, and miR26b [30, 31, 32, 33, 34]. [score:3]
MiR-208, together with miR-1, miR-133, and miR-206, are called myomiRs as they are expressed specifically in the heart and skeletal muscles. [score:3]
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This expression profile was not observed for a group of well-known cardiac or muscle specific miRNAs (miR-1, miR-133a, miR-133b, miR-208a, miR-208b, miR-499-5p and miR-499-3p). [score:3]
Expression profile of (A) miRNA-940; (B) miR-1; (C) miR-133a; (D) miR-133b; (E) miR-499-3p; (F) miR-499-5p; (G) miR-208a; (H) miR-208b in different part of human hearts. [score:3]
Furthermore, compared to well-known cardiac or muscle specific miRNAs (miR-1, miR-133a, miR-133b, miR-208a, miR-208b, miR-499-5p and miR-499-3p), miRNA-940 was the only one which is most highly expressed in the normal human right ventricular out-flow tract comparing to other chambers within the heart (Fig. 3). [score:2]
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35
[+] score: 8
miR-208a-3p suppresses cell apoptosis by targeting PDCD4 in gastric cancer. [score:5]
For example, miR-208a-3p promotes gastric cancer cell proliferation via targeting PDCD4 3′-UTR (Yin et al., 2016). [score:3]
[1 to 20 of 2 sentences]
36
[+] score: 8
It is noteworthy that five miRNAs (hsa-miR-208a, -519d, -605, -634, -99b*) were found to be up-regulated only in large artery stroke samples (BB, DB, E, LB, LC, LX; Table 2). [score:4]
Of these miRNAs, only miR-208a and miR-636 exhibited opposite profile in DB (mRS = 4; Table 3) while the other 25 miRNAs were upregulated in the large artery stroke samples with mRS ≤ 2 (Table 3). [score:4]
[1 to 20 of 2 sentences]
37
[+] score: 7
The up-regulated miRNAs include let-7a and miR-99a and the down-regulated include miR-196a, miR-470, miR-21*, miR-208a, miR-683, miR-184, miR-693-3p, miR-202-3p, miR-429, miR-878-3p and miR-327. [score:7]
[1 to 20 of 1 sentences]
38
[+] score: 7
A 10-fold increase in miRNA -mediated murine cardiac fibroblast reprogramming was observed when miRNA-1, miRNA-133, miRNA-208, and miRNA-499 were combined with JAK inhibitor I [30]. [score:3]
miRNA-1, miRNA-133, miRNA-208, and miRNA-499 have been shown to be cardiac- and muscle-specific and play important roles in cardiac development and function. [score:2]
A combination of miRNA-1, miRNA-133, miRNA-208, and miRNA-499 was reported to be sufficient to convert mouse cardiac fibroblasts into iCMs without the addition of other factors in vivo [36]. [score:1]
Zhao et al. used a combination of GMHT, miRNA-1, miRNA-133, miRNA-208, miRNA-499, Y-27632, and A83-01 in MEFs and mouse adult fibroblasts to achieve ~60% cardiac troponin T+ and 60% α-actinin+ iCMs [29]. [score:1]
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39
[+] score: 7
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]
Using an elegant transgenic mouse mo del, they demonstrated that miR-208a is required for expression of β-MHC/miR-499 but its cardiac functions can be replaced by miR-499, suggesting the latter as a downstream mediator. [score:3]
[1 to 20 of 2 sentences]
40
[+] score: 7
Recently, we reported that overexpression of miR-208a in the heart, which is normally restricted to cardiac tissue, was sufficient to induce cardiac hypertrophy in transgenic mice [34]. [score:3]
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 3 sentences]
41
[+] score: 7
In line with these results, we found that miR-208a-3p and miR-499-5p -both cardiac specific and highly abundant in the heart [23]- were either undetectable or very lowly expressed in the circulation of mice. [score:3]
In addition to the cardiac specific miR-208a-3p and miR-499-5p, we found that the expression of let-7i-5p, miR-16-5p, miR-27a-3p, miR-199a-3p and miR-223-3p was significantly higher in the heart compared to the kidney, independent of the presence of ischemic heart failure (S4 Fig and S5 Table). [score:2]
Of the cardiac specific miRNAs, miR-208a-3p was not detectable in the plasma of ischemic heart failure mice and miR-499-5p showed the lowest miRNA expression levels in plasma compared to the other miRNAs (Fig 3 and S4 Table). [score:2]
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42
[+] score: 7
Several miR -based therapeutics are already in development in the cardio-metabolic context, including an antisense inhibitor of miR-208a, which offers improved recovery from heart failure in animal mo dels (Miragen Therapeutics Inc. [score:4]
Therapeutic inhibition of miR-208a improves cardiac function and survival during heart failure. [score:3]
[1 to 20 of 2 sentences]
43
[+] score: 7
miR-133 and miR-208 converge around structures pertaining to myocardial tissue albeit with opposite effects on cardiac hypertrophy, as miR-133 yields both anti-fibrotic and anti-hypertrophic effects [14], whereas overexpression of miR-208 is pro-hypertrophic [15]. [score:3]
miRs studied included miR-17, miR-92a, miR-126, miR-34, miR-181b, miR-221, miR-222 (endothelium related), miR-208, 133 (myocardium related), miR-21, miR-145 (vascular smooth muscle related), and miR-155 (Inflammatory cell related). [score:1]
In particular, an absolute and relative decrease in endothelial-related miRs (miR-17, miR-92a, miR-126), smooth muscle miR (miR-145), and inflammatory cell -mediated miR (miR-155) with a converse increase in miR-133a and miR-208a (myocardial -associated miRs) was observed in patients with stable CHD [22]. [score:1]
A recent study uncovered an association between a series of miRs specific to the myocardium (miR-133a, miR-208a), the vasculature (miR-17, miR-92a, miR-126), inflammatory cells (miR-145), smooth muscle and (miR-155) and the presence of stable CHD [22]. [score:1]
On the other hand, in patients with active acute coronary syndromes (ACS) miR-133a and miR-208a (myocardial miRs), miR-126 and miR-92a (endothelial), and miR-155 (inflammatory cell) levels were all found to be increased in aortic blood samples (miR-133a, miR-208a also increased in coronary sinus samples), with increased transcoronary gradient of miR-133 and trends toward negative gradients of miR-92a and miR-126 [23]. [score:1]
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44
[+] score: 6
Circulating miR-1, miR-208a and miR-133a are overexpressed in the following 2 h after an acute myocardial infarction [106], and circulating miR-423-5p is upregulated in heart failure [107, 108]. [score:6]
[1 to 20 of 1 sentences]
45
[+] score: 6
We then analyzed the GO terms associated to targets of the microRNA families highly expressed in CM, including miR-1 (mir-1 and mir-206), miR-133 (miR-133a and b), miR-208 (miR-208a and b), miR-490, miR-499 and miR-143. [score:5]
Some of these microRNAS have been previously reported and are well-known in the context of cardiac differentiation, such as hsa-mir-1-3p, hsa-mir-499-5p, and the mir-208 and mir-133 families 39, 40. [score:1]
[1 to 20 of 2 sentences]
46
[+] score: 6
Among these three miRNAs, miR-208a is specifically expressed only in cardiac muscle, whereas miR-208b and miR-499 are also expressed in type I (slow) muscle fibers [67]. [score:5]
These intronic miRNAs, miR-208a, miR-208b, and miR-499, are embedded in three muscle-specific MyHC genes (Myh6, Myh7, and Myh7b, resp. ) [score:1]
[1 to 20 of 2 sentences]
47
[+] 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]
48
[+] score: 6
Recent studies found that the expression of miRNAs can be regulated by insulin such as miR-208 which played a role in insulin -induced VSMC proliferation by p21, a key member of CDK -inhibitory protein family [13]. [score:6]
[1 to 20 of 1 sentences]
49
[+] score: 6
Other miRNAs like miR-138, miR-375, miR-593, miR-133a were down-regulated in esophageal cancer tissue, serving as tumor suppressors, while miR-34b, miR-16, miR-208, miR-423, miR-21, miR-31, miR-223 and miR-373 could have oncogenic actions [18– 23] (Figure 1). [score:6]
[1 to 20 of 1 sentences]
50
[+] score: 6
The expression of miR-23a, miR-181c, miR-192, miR-194, miR-208, miR-337-5p, miR-338-3p, miR-502-5p, miR-542-3p, miR-628-5p, and miR-672 is upregulated in the oral mucosa of heavy smokers with lung cancer versus patients without cancer and light smokers [66]. [score:6]
[1 to 20 of 1 sentences]
51
[+] score: 6
We determined the expression of angiogenesis-related miRNAs (miR-20a, miR-126, miR-210, miR-221, miR-222, miR-328; Dews et al., 2006; Poliseno et al., 2006; Kuehbacher et al., 2007; Fasanaro et al., 2008; Soeki et al., 2016), inflammation-related miRNAs (miR-21, miR-146a, miR-155; Taganov et al., 2006; Urbich et al., 2008; Wang et al., 2017) and cardiac or muscle-specific/enriched miRNAs (miR-1, miR-133a, miR-133b, miR-208a, miR-208b, miR-378, miR-486, miR-499, miR-940; Chen et al., 2006; Soci et al., 2016; Xu et al., 2016). [score:3]
MicroRNA208 family in cardiovascular diseases: therapeutic implication and potential biomarker. [score:2]
Epigenetic control of exercise training -induced cardiac hypertrophy by miR-208. [score:1]
[1 to 20 of 3 sentences]
52
[+] score: 6
miR-ID Increased Fold-Changes miR-ID Decreased Fold-Changes miR-29b 8.5 miR-17 15.7 miR-29a 7.7 miR-92a 13.6 miR-29c 7.3 miR-18a 12.0 miR-1224 6.6 miR-192 7.2 miR-133b 2.0 miR-127 2.4 miR-200c 1.7 miR-154 1.9 miR-200a 1.4 miR-21 1.7 miR-205 1.3 miR-680 1.3 miR-208a 1.2 miR-377 1.2 miR-669b 1.2 miR-153 1.1 Figure 3Fucoidan increases the expression of miR-29b. [score:3]
miR-ID Increased Fold-Changes miR-ID Decreased Fold-Changes miR-29b 8.5 miR-17 15.7 miR-29a 7.7 miR-92a 13.6 miR-29c 7.3 miR-18a 12.0 miR-1224 6.6 miR-192 7.2 miR-133b 2.0 miR-127 2.4 miR-200c 1.7 miR-154 1.9 miR-200a 1.4 miR-21 1.7 miR-205 1.3 miR-680 1.3 miR-208a 1.2 miR-377 1.2 miR-669b 1.2 miR-153 1.1 Figure 3Fucoidan increases the expression of miR-29b. [score:3]
[1 to 20 of 2 sentences]
53
[+] score: 6
Conversely, inhibition of mir-208a (upregulated 12.4 fold in adult CPCs) reduced cardiac remo deling, improved cardiac function, and survival after hypertension -induced heart failure [53]. [score:6]
[1 to 20 of 1 sentences]
54
[+] score: 5
Twelve of 116 TS miRNAs (miR-1, miR-126, miR-208, miR-128a, miR-133a, miR-133b, miR-134, miR-146a, miR-377, miR-483, miR-92a and miR-95) were specifically expressed in two tissues; whereas, the remaining TS miRNAs were specifically expressed in only one tissue. [score:5]
[1 to 20 of 1 sentences]
55
[+] score: 5
In particular, miR-208a repressed endoglin expression in the heart, whereas miR-370 was negatively correlated with endoglin expression in endometrioid ovarian cancer cells. [score:5]
[1 to 20 of 1 sentences]
56
[+] score: 5
The present findings revealed that miRNA-21 and miRNA-208 are highly expressed in patients with AF, though there were no significant differences between AF and SR patients regarding miRNA-133 and miRNA-590 expressions. [score:5]
[1 to 20 of 1 sentences]
57
[+] score: 5
Some micro (mi)RNAs, such as miRNA-1, miRNA-133, and miRNA-208, have been demonstrated to be involved with gene regulation properties and specific expression profiles, and imbalances can be found in chagasic cardiomyopathy (13). [score:4]
Study Source Biomarker name Result Reference Experimental, parasitemia-specific Antigenic Aptamer Increased levels(39, 40) Chagasic cardiomyopathy Genetic CCL2 and MAL/TIRAP Increased susceptibility(41) Chagasic cardiomyopathy Genetic CCR5 Protection(41) Chagasic cardiomyopathy Phenotype CD15s+ Treg cells Protection(35, 36) Chagasic cardiomyopathy Phenotype CD27+CD28+CD8+ T cells Protection(37, 38) Non-specific Plasmatic TIMP-1 and TIMP-2 Increased levels(5, 6) Non-specific Plasmatic Troponin I Increased levels(5, 6) Non-specific Plasmatic TGF-β Increased levels(5, 6) Asymptomatic Plasmatic IL-10 Increased levels(11) Non-specific Plasmatic APOA1 Decreased levels(7) Non-specific Plasmatic Fibronectin Increased levels(7) Asymptomatic Plasmatic MMP-2 Increased levels(14) Chagasic cardiomyopathy Plasmatic MMP-9 Increased levels(14) Chagasic cardiomyopathy Plasmatic ANP, BNP, N-terminal pro-BNP, IFN-γ, TNF-α, IL-1β, and IL-6 Increased levels(4, 8, 10, 11) Chagasic cardiomyopathy Plasmatic miRNA-1, miRNA-133a and -133b, and miRNA-208a and -208b Decreased levels(13) Experimental, chagasic cardiomyopathy Plasmatic PICP and PIIINP Increased levels(15) Experimental, chagasic cardiomyopathy Plasmatic Syndecan-4, ICAM-1, and Galectin-3 Increased levels(16) Efficacy Management KMP11, HSP70, PAR2, and Tgp63 Increased Ab. [score:1]
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58
[+] score: 5
For example, miR-208 and miR-499 are cardiac-specific miRNAs exclusively expressed in cardiac tissues, while miR-1 and miR-133 are muscle-specific miRNAs preferentially expressed in cardiac and skeletal muscle [37, 38]. [score:5]
[1 to 20 of 1 sentences]
59
[+] score: 5
Among them, a miR-208a antimiR has been shown to suppress fibrosis by reducing myosin 7 expression and improve survival in Dahl salt-sensitive rats [49]. [score:5]
[1 to 20 of 1 sentences]
60
[+] score: 5
Interventional cardiologists have already provided evidence that cardiac expressed miRs (miR-1, miR-133a, miR-133b, miR-208a, miR-208b, and miR-499) increase in the blood acutely following a myocardial infarction (MI) and some of these studies have additionally scrutinized the diagnostic potential of miRs by comparisons with cTns[15– 17]. [score:3]
Similarly, miR-1 and miR-208a increased at 45 min after aortic clamping in patients undergoing combined mitral and aortic valve replacement[25]. [score:1]
Cardiac-expressed (miR-1, miR-24, miR-133a/b, miR-208a/b, miR-210), non-cardiovascular (miR-122) and quality control miRs were measured in whole plasma and in plasma exosomes. [score:1]
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61
[+] score: 5
The rest of the miRNAs assayed were detected in most or all of the tissues by both methods, with two exceptions: miR-208, expressed only in the heart [34] and at very low levels in skeletal muscle, and miR-138, expressed in the brain, and at lower levels in placenta and thymus (all data is shown in Additional File 1). [score:4]
Third, we chose several miRNAs which had potentially problematic sequences or exhibited atypical behavior during the development of the Agilent microarray platform: two of these did not show as good a linear titration curve as other miRNAs tested in a previous study (miR-126*, miR-296) [26], and two other miRNAs were previously reported not to be labeled by enzymatic methods similar (but not identical) to that used with the Agilent microarray assay (miR-208, miR-219) [33]. [score:1]
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62
[+] score: 4
For example, miR-150 was found to be reduced in serum of patients with arterial fibrillation and miR-1, miR-134, miR-186, miR-208, miR-233 and miR-499 were all found to be significantly upregulated in serum from acute myocardial infarction (AMI) patients [22- 24]. [score:4]
[1 to 20 of 1 sentences]
63
[+] score: 4
Other miRNAs from this paper: hsa-mir-10b, hsa-mir-208b
The finding that the expression of E-cadherin is decreased by Nrf2 activation already on the mRNA level indicated that Nrf2 either directly affects activation of the E-cadherin promoter or that Nrf2 exerts epigenetic effects, e. g. through miRs like miR-10b or miR-208. [score:4]
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64
[+] score: 4
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]
Interestingly, mice lacking the cardiac-specific microRNA miR-208a have decreased amounts of miR-499 [25], [36]. [score:1]
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 3 sentences]
65
[+] score: 4
Other miRNAs from this paper: hsa-mir-22, hsa-mir-23a, hsa-mir-1-2, hsa-mir-145, hsa-mir-195
Of the previously established hypertrophy miRNAs, we found hsa-miR-23a-3p, hsa-miR-22-3p and hsa-miR-208a-3p to have significant differential expression. [score:3]
We also observe miRNAs with moderate abundance, hsa-mir-22-3p, hsa-mir-208a-3p in addition to low abundant transcripts like hsa-mir-195. [score:1]
[1 to 20 of 2 sentences]
66
[+] score: 4
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-17, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26a-1, hsa-mir-27a, hsa-mir-29a, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-10a, hsa-mir-181a-2, hsa-mir-181c, hsa-mir-199a-2, hsa-mir-181a-1, hsa-mir-214, hsa-mir-221, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-23b, hsa-mir-27b, hsa-mir-125b-1, hsa-mir-128-1, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-143, hsa-mir-125b-2, hsa-mir-126, hsa-mir-127, hsa-mir-206, hsa-mir-1-1, hsa-mir-128-2, hsa-mir-29c, hsa-mir-26a-2, hsa-mir-378a, hsa-mir-148b, hsa-mir-133b, hsa-mir-424, ssc-mir-125b-2, ssc-mir-148a, ssc-mir-23a, ssc-mir-24-1, ssc-mir-26a, ssc-mir-29b-1, ssc-mir-181c, ssc-mir-214, ssc-mir-27a, ssc-let-7c, ssc-let-7f-1, ssc-let-7i, ssc-mir-103-1, ssc-mir-128-1, ssc-mir-29c, hsa-mir-486-1, hsa-mir-499a, hsa-mir-503, hsa-mir-411, hsa-mir-378d-2, hsa-mir-208b, hsa-mir-103b-1, hsa-mir-103b-2, ssc-mir-17, ssc-mir-221, ssc-mir-133a-1, ssc-mir-1, ssc-mir-503, ssc-mir-181a-1, ssc-mir-206, ssc-let-7a-1, ssc-let-7e, ssc-let-7g, ssc-mir-378-1, ssc-mir-133b, ssc-mir-29a, ssc-mir-199a-2, ssc-mir-128-2, ssc-mir-499, ssc-mir-143, ssc-mir-10a, ssc-mir-486-1, ssc-mir-103-2, ssc-mir-181a-2, ssc-mir-27b, ssc-mir-24-2, ssc-mir-23b, ssc-mir-148b, ssc-mir-208b, ssc-mir-424, ssc-mir-127, ssc-mir-125b-1, hsa-mir-378b, hsa-mir-378c, ssc-mir-411, ssc-mir-133a-2, ssc-mir-126, ssc-mir-199a-1, ssc-mir-378-2, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-499b, ssc-let-7a-2, ssc-mir-486-2, hsa-mir-378j, ssc-let-7d, ssc-let-7f-2, ssc-mir-29b-2, hsa-mir-486-2, ssc-mir-378b
Exceptions were some previously reported muscle-related miRNAs such as miR-181c/d-5p, miR-29b/c, miR-221/222 and miR-208, all of which expressed at a very low level (average RPM <100). [score:3]
In addition to the best-studied myomiRs (miR-1, -206 and miR-133 families), 11 other DE muscle-related miRNAs (miR-378 [24], miR-148a [27], miR-26a [28, 29], miR-27a/b [30, 31], miR-23a [32, 33], miR-125b [34], miR-24 [35], miR-128 [36], miR-199a [37] and miR-424 [38]) with high abundance (average RPM >1,000) and another 14 (miR-181a/b/c/d-5p [26], miR-499-5p [11], miR-503 [38], miR-486 [39], miR-214 [40], miR-29a/b/c [41– 43], miR-221/222 [44] and miR-208 [11] with low abundance (average RPM <1,000) were detected in myogenesis of pig. [score:1]
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67
[+] score: 4
Furthermore, miR-133a and miR-208a (cardiac-muscle miRNAs) were significantly upregulated. [score:4]
[1 to 20 of 1 sentences]
68
[+] score: 4
The expression of muscle-specific myosin genes is regulated by a group of intronic miRNAs, including miR-208a, miR-208b and miR-499, which are embedded within the introns of Myh6, Myh7 and Myh7b, respectively [74]. [score:4]
[1 to 20 of 1 sentences]
69
[+] score: 4
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-29a, hsa-mir-31, hsa-mir-99a, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, hsa-mir-16-2, hsa-mir-192, hsa-mir-199a-1, hsa-mir-30c-2, hsa-mir-147a, hsa-mir-10a, hsa-mir-34a, hsa-mir-181b-1, hsa-mir-199a-2, hsa-mir-203a, hsa-mir-204, hsa-mir-217, hsa-mir-219a-1, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-mir-200b, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-125b-1, hsa-mir-132, hsa-mir-140, hsa-mir-142, hsa-mir-143, hsa-mir-145, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-146a, hsa-mir-150, hsa-mir-185, hsa-mir-193a, hsa-mir-195, hsa-mir-200c, hsa-mir-155, hsa-mir-181b-2, hsa-mir-30c-1, hsa-mir-219a-2, hsa-mir-296, hsa-mir-130b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-302d, hsa-mir-374a, hsa-mir-375, hsa-mir-378a, hsa-mir-330, hsa-mir-328, hsa-mir-342, hsa-mir-325, hsa-mir-424, hsa-mir-429, hsa-mir-450a-1, hsa-mir-486-1, hsa-mir-146b, hsa-mir-497, hsa-mir-520e, hsa-mir-520f, hsa-mir-520a, hsa-mir-520b, hsa-mir-520c, hsa-mir-520d, hsa-mir-520g, hsa-mir-520h, hsa-mir-450a-2, hsa-mir-503, hsa-mir-608, hsa-mir-625, hsa-mir-629, hsa-mir-663a, hsa-mir-1271, hsa-mir-769, hsa-mir-378d-2, hsa-mir-675, hsa-mir-147b, hsa-mir-374b, hsa-mir-663b, hsa-mir-378b, hsa-mir-378c, hsa-mir-374c, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-4661, hsa-mir-219b, hsa-mir-203b, hsa-mir-378j, hsa-mir-486-2
In this context, Recchiuti et al. [113] verified that miR-21, miR-146b, miR-142 family, miR-203, miR-208a, miR-219, and miR-302d that are temporally and differentially expressed in resolving exudates, and Resolvin D1, which is biosynthesized in resolution, regulates miR-21, miR-146b, miR-208a, and miR-219. [score:4]
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70
[+] score: 4
As to pathological changes, tissue specific miRNAs were analyzed in the blood stream as markers for myocardial injury and drug induced liver injury: A rat mo del of acute myocardial infarction demonstrated that the plasma levels of the cardiac-specific miRNA-208 and miRNA-499 are increased in this disease [50]. [score:3]
For example, miRNA-208 was shown to be exclusively expressed in the heart and was measured in the serum after heart tissue injury [29]. [score:1]
[1 to 20 of 2 sentences]
71
[+] score: 4
Sun et al. have demonstrated that miR-208a-SOX2/β-catenin-Lin28-let-7a-DICER1 regulatory feedback loop participates in the therapy resistance of breast cancer through promoting the induction of the cancer stem cells [56]. [score:2]
Based on the Figure 5 of their work, miR-208a increased the activity of DICER1 while let-7a directly targeted and degraded DICER1 mRNA, it is necessary to investigate whether the observation could be explained by the competitive endogenous RNA (ceRNA) hypothesis. [score:2]
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72
[+] score: 3
1. Tang Y Cui Y Li Z Jiao Z Zhang Y He Y Radiation -induced miR-208a increases the proliferation and radioresistance by targeting p21 in human lung cancer cellsJ Exp Clin Cancer Res. [score:3]
[1 to 20 of 1 sentences]
73
[+] score: 3
Here, miR-208a, whose association with breast cancer is not reported in any research study, is proposed as a new miRNA that is associated with this disease. [score:3]
[1 to 20 of 1 sentences]
74
[+] score: 3
The mean expression of only two of the Affymetrix U133A probes was significantly different between groups (ELM2 hosting miR-330 with p = 0.03; MYH6 hosting miR-208 with p = 0.03). [score:3]
[1 to 20 of 1 sentences]
75
[+] score: 3
MyomiRs (miR-1, miR-133, miR-206, miR-208, miR-486 and miR-499) are highly enriched in cardiac and skeletal muscle, miR-1 being the most abundant miRNA in the heart [44]. [score:1]
They include miR-1, miR-133, miR-206 (skeletal muscle only), miR-208, miR-486 and miR-499 [27]. [score:1]
MiR-208a and miR-208 were recorded in 6% and 4% of samples, respectively. [score:1]
[1 to 20 of 3 sentences]
76
[+] score: 3
Recent studies suggest that circulating miRNAs may represent a new class of biomarkers for monitoring the progress of certain diseases [13– 20], such as miR-9 as novel noninvasive molecular marker for traumatic spinal cord injury [14], miR-208a for early detection of acute myocardial infarction [15], and miR-146a/223 for the diagnosis of sepsis [16]. [score:3]
[1 to 20 of 1 sentences]
77
[+] score: 3
The targets of some miRNAs were strongly enriched in certain categories, e. g., miR-105 in “small GTPase mediated signal transduction” (5-fold), miR-208 in “transcription factor” (6-fold), and miR-7, which lies in the intron of the hnRNPk (an RNA -binding protein) gene, in “RNA binding proteins. [score:3]
[1 to 20 of 1 sentences]
78
[+] 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]
79
[+] score: 3
From the 7 microRNAs assessed, miR-133a, miR-21 and miR-19b were detected both in myocardial and serum samples from AS patients and control subjects, whereas the expression of miR-29b, miR-1, miR-208a and miR-499-5p was under the limit of detection in serum samples from AS patients and control subjects. [score:3]
[1 to 20 of 1 sentences]
80
[+] score: 3
Thus far, the 10 miRNAs, that is, hsa-miR-6804-3p, hsa-miR-4289, hsa-miR-208a-3p, hsa-miR-510-3p, hsa-miR-329-3p, hsa-miR-548ax, hsa-miR-3934-5p, hsa-miR-4474-5p, hsa-miR-7974, and hsa-miR-6865-5p, do not have any known function in human and other animals. [score:1]
The utility of those 13 miRNAs, that is, hsa-miR-628-5p, hsa-miR-6804-3p, hsa-miR-4289, hsa-miR-208a-3p, hsa-miR-510-3p, hsa-miR-18a-3p, hsa-miR-329-3p, hsa-miR-548ax, hsa-miR-3934-5p, hsa-miR-4474-5p, hsa-miR-7974, hsa-miR-6865-5p, and hsa-miR-342-3p, can be utilized as antiviral therapeutics against MERS-CoV infection. [score:1]
Other hairpins MD5, MD17, MD157, MD244, MD366, MR175, MR201, MR268, and MR282 were aligned with hsa-miR-628-5p, hsa-miR-6804-3p, hsa-miR-4289, hsa-miR-208a-3p, hsa-miR-510-3p, hsa-miR-18a-3p, hsa-miR-329-3p, hsa-miR-548ax, and hsa-miR-342-3p, respectively. [score:1]
[1 to 20 of 3 sentences]
81
[+] score: 3
The heart expresses miR-1, miR-133, miR-206, and specifically miR-208 [45, 46]. [score:3]
[1 to 20 of 1 sentences]
82
[+] score: 3
Focusing on the involvement of miRNAs in muscle development and myogenesis, a restricted group of muscle-enriched miRNAs, also called myomiRs (miR-1, miR-133, miR-206 and miR-208), was demonstrated fundamental for muscle physiology and plasticity [9], [10], [11]. [score:2]
Following the discovery of miRNAs, their participation was investigated in almost all biological processes and, even more importantly, their central role in gene -expression regulation was implicated in many human diseases [3], [4], [5], [6], [7], [8] Regarding this, in the recent years many efforts were focused to finely characterize the role of miRNAs in myogenesis, so that now the miRNA biogenesis is considered necessary for proper muscle development and a restricted number of miRNAs, known as myomiRs (miR-1, miR-133, miR-181, miR-206, miR-208), is considered as integral part of muscle biology [9], [11]. [score:1]
[1 to 20 of 2 sentences]
83
[+] score: 3
Other miRNAs from this paper: hsa-mir-375
Furthermore, experimental evidences such as miR-208a-MED13 axis showing a potential linkage between metabolic disorders such as type 2 diabetes, obesity, and cardiovascular disease can be seen [13]. [score:3]
[1 to 20 of 1 sentences]
84
[+] score: 3
Nabiałek E Wańha W Kula D Circulating microRNAs (miR-423-5p, miR-208a and miR-1) in acute myocardial infarction and stable coronary heart disease. [score:3]
[1 to 20 of 1 sentences]
85
[+] score: 3
Tang Y Radiation -induced miR-208a increases the proliferation and radioresistance by targeting p21 in human lung cancer cellsJ. [score:3]
[1 to 20 of 1 sentences]
86
[+] 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]
87
[+] 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]
88
[+] score: 3
Other miRNAs from this paper: hsa-mir-21, hsa-mir-27b, hsa-mir-423
Among the number of miRNAs identified to be differentially regulated, the miRNAs significantly changed were miR21, miR208a, miR423 and miR27b that have been shown to regulate endothelial and myogenic differentiation. [score:3]
[1 to 20 of 1 sentences]
89
[+] score: 2
It was reported that cardiomyocytes-derived miRNAs (miR-1, miR-208, miR-499, miR-133, miR-30c, miR-181, etc. ) [score:1]
A series of studies have demonstrated that cardiomyocytes specific miRNAs (miR-1, miR-208, miR-499, miR-133, etc. ) [score:1]
[1 to 20 of 2 sentences]
90
[+] score: 2
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-21, hsa-mir-22, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-27a, hsa-mir-30a, hsa-mir-31, hsa-mir-98, hsa-mir-99a, hsa-mir-101-1, hsa-mir-16-2, hsa-mir-192, hsa-mir-197, hsa-mir-199a-1, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-10a, hsa-mir-10b, hsa-mir-34a, hsa-mir-187, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-203a, hsa-mir-211, hsa-mir-219a-1, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-mir-224, hsa-mir-200b, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-128-1, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-138-2, hsa-mir-140, hsa-mir-142, hsa-mir-143, hsa-mir-144, hsa-mir-145, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-138-1, hsa-mir-146a, hsa-mir-200c, hsa-mir-155, hsa-mir-128-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-101-2, hsa-mir-219a-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-99b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-375, hsa-mir-328, hsa-mir-337, hsa-mir-338, hsa-mir-339, hsa-mir-384, hsa-mir-424, hsa-mir-429, hsa-mir-449a, hsa-mir-485, hsa-mir-146b, hsa-mir-494, hsa-mir-497, hsa-mir-498, hsa-mir-520a, hsa-mir-518f, hsa-mir-499a, hsa-mir-509-1, hsa-mir-574, hsa-mir-582, hsa-mir-606, hsa-mir-629, hsa-mir-449b, hsa-mir-449c, hsa-mir-509-2, hsa-mir-874, hsa-mir-744, hsa-mir-208b, hsa-mir-509-3, hsa-mir-1246, hsa-mir-1248, hsa-mir-219b, hsa-mir-203b, hsa-mir-499b
Moreover, in the same study the expression of HS_101, HS_206, miR-208, miR-518f, and miR-606 were increased in patients with allergic asthma as compared to non-allergic subjects. [score:2]
[1 to 20 of 1 sentences]
91
[+] score: 2
Other miRNAs from this paper: hsa-mir-17, hsa-mir-19a, hsa-mir-29a, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-198, hsa-mir-10a, hsa-mir-223, hsa-mir-122, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125b-2, hsa-mir-126, hsa-mir-146a, hsa-mir-150, hsa-mir-155, hsa-mir-29c, hsa-mir-99b, hsa-mir-296, hsa-mir-196b, hsa-mir-515-1, hsa-mir-515-2, hsa-mir-548a-1, hsa-mir-548b, hsa-mir-548a-2, hsa-mir-550a-1, hsa-mir-550a-2, hsa-mir-548a-3, hsa-mir-548c, hsa-mir-640, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-550a-3, bta-mir-29a, bta-mir-125b-1, bta-mir-126, bta-mir-10a, bta-mir-124a-1, bta-mir-17, bta-mir-29b-2, bta-mir-29c, bta-mir-150, bta-mir-122, bta-mir-125b-2, bta-mir-19a, bta-mir-99b, hsa-mir-208b, hsa-mir-548e, hsa-mir-548j, hsa-mir-548k, hsa-mir-548l, hsa-mir-548f-1, hsa-mir-548f-2, hsa-mir-548f-3, hsa-mir-548f-4, hsa-mir-548f-5, hsa-mir-548g, hsa-mir-548n, hsa-mir-548m, hsa-mir-548o, hsa-mir-548h-1, hsa-mir-548h-2, hsa-mir-548h-3, hsa-mir-548h-4, hsa-mir-548p, hsa-mir-548i-1, hsa-mir-548i-2, hsa-mir-548i-3, hsa-mir-548i-4, bta-mir-124a-2, bta-mir-124b, bta-mir-146a, bta-mir-155, bta-mir-196b, bta-mir-208a, bta-mir-208b, bta-mir-223, bta-mir-296, bta-mir-29d, bta-mir-9-1, bta-mir-9-2, bta-mir-29e, bta-mir-29b-1, hsa-mir-548q, bta-mir-2284i, bta-mir-2285a, bta-mir-2284s, bta-mir-2285d, bta-mir-2284l, bta-mir-2284j, bta-mir-2284t, bta-mir-2285b-1, bta-mir-2284d, bta-mir-2284n, bta-mir-2284g, bta-mir-2284p, bta-mir-2284u, bta-mir-2284f, bta-mir-2284a, bta-mir-2284k, bta-mir-2284c, bta-mir-2284v, bta-mir-2285c, bta-mir-2284q, bta-mir-2284m, bta-mir-2284b, bta-mir-2284r, bta-mir-2284h, bta-mir-2284o, bta-mir-2284e, hsa-mir-548s, hsa-mir-548t, hsa-mir-548u, hsa-mir-548v, hsa-mir-548w, hsa-mir-548x, bta-mir-2284w, bta-mir-2284x, hsa-mir-548y, hsa-mir-550b-1, hsa-mir-550b-2, hsa-mir-548z, hsa-mir-548aa-1, hsa-mir-548aa-2, hsa-mir-548o-2, hsa-mir-548h-5, hsa-mir-548ab, hsa-mir-548ac, hsa-mir-548ad, hsa-mir-548ae-1, hsa-mir-548ae-2, hsa-mir-548ag-1, hsa-mir-548ag-2, hsa-mir-548ah, hsa-mir-548ai, hsa-mir-548aj-1, hsa-mir-548aj-2, hsa-mir-548x-2, hsa-mir-548ak, hsa-mir-548al, hsa-mir-548am, hsa-mir-548an, hsa-mir-548ao, hsa-mir-548ap, hsa-mir-548aq, hsa-mir-548ar, hsa-mir-548as, hsa-mir-548at, hsa-mir-548au, hsa-mir-548av, hsa-mir-548aw, hsa-mir-548ax, bta-mir-2284y-1, bta-mir-2285e-1, bta-mir-2285e-2, bta-mir-2285f-1, bta-mir-2285f-2, bta-mir-2285g-1, bta-mir-2285h, bta-mir-2285i, bta-mir-2285j-1, bta-mir-2285j-2, bta-mir-2285k-1, bta-mir-2285l, hsa-mir-548ay, hsa-mir-548az, bta-mir-2285o-1, bta-mir-2285o-2, bta-mir-2285n-1, bta-mir-2285n-2, bta-mir-2285p, bta-mir-2285m-1, bta-mir-2285m-2, bta-mir-2284y-2, bta-mir-2285n-3, bta-mir-2285n-4, bta-mir-2284y-3, bta-mir-2285o-3, bta-mir-2285o-4, bta-mir-2285m-3, bta-mir-2284y-4, bta-mir-2284y-5, bta-mir-2284y-6, bta-mir-2285m-4, bta-mir-2285o-5, bta-mir-2285m-5, bta-mir-2285n-5, bta-mir-2285n-6, bta-mir-2284y-7, bta-mir-2285n-7, bta-mir-2284z-1, bta-mir-2284aa-1, bta-mir-2285k-2, bta-mir-2284z-3, bta-mir-2284aa-2, bta-mir-2284aa-3, bta-mir-2285k-3, bta-mir-2285k-4, bta-mir-2284z-4, bta-mir-2285k-5, bta-mir-2284z-5, bta-mir-2284z-6, bta-mir-2284z-7, bta-mir-2284aa-4, bta-mir-2285q, bta-mir-2285r, bta-mir-2285s, bta-mir-2285t, bta-mir-2285b-2, bta-mir-2285v, bta-mir-2284z-2, bta-mir-2285g-2, bta-mir-2285g-3, bta-mir-2285af-1, bta-mir-2285af-2, bta-mir-2285y, bta-mir-2285w, bta-mir-2285x, bta-mir-2285z, bta-mir-2285u, bta-mir-2285aa, bta-mir-2285ab, bta-mir-2284ab, bta-mir-2285ac, bta-mir-2285ad, bta-mir-2284ac, bta-mir-2285ae, hsa-mir-548ba, hsa-mir-548bb, hsa-mir-548bc, bta-mir-2285ag, bta-mir-2285ah, bta-mir-2285ai, bta-mir-2285aj, bta-mir-2285ak, bta-mir-2285al, bta-mir-2285am, bta-mir-2285ar, bta-mir-2285as-1, bta-mir-2285as-2, bta-mir-2285as-3, bta-mir-2285at-1, bta-mir-2285at-2, bta-mir-2285at-3, bta-mir-2285at-4, bta-mir-2285au, bta-mir-2285av, bta-mir-2285aw, bta-mir-2285ax-1, bta-mir-2285ax-2, bta-mir-2285ax-3, bta-mir-2285ay, bta-mir-2285az, bta-mir-2285an, bta-mir-2285ao-1, bta-mir-2285ao-2, bta-mir-2285ap, bta-mir-2285ao-3, bta-mir-2285aq-1, bta-mir-2285aq-2, bta-mir-2285ba-1, bta-mir-2285ba-2, bta-mir-2285bb, bta-mir-2285bc, bta-mir-2285bd, bta-mir-2285be, bta-mir-2285bf-1, bta-mir-2285bf-2, bta-mir-2285bf-3, bta-mir-2285bg, bta-mir-2285bh, bta-mir-2285bi-1, bta-mir-2285bi-2, bta-mir-2285bj-1, bta-mir-2285bj-2, bta-mir-2285bk, bta-mir-2285bl, bta-mir-2285bm, bta-mir-2285bn, bta-mir-2285bo, bta-mir-2285bp, bta-mir-2285bq, bta-mir-2285br, bta-mir-2285bs, bta-mir-2285bt, bta-mir-2285bu-1, bta-mir-2285bu-2, bta-mir-2285bv, bta-mir-2285bw, bta-mir-2285bx, bta-mir-2285by, bta-mir-2285bz, bta-mir-2285ca, bta-mir-2285cb, bta-mir-2285cc, bta-mir-2285cd, bta-mir-2285ce, bta-mir-2285cf, bta-mir-2285cg, bta-mir-2285ch, bta-mir-2285ci, bta-mir-2285cj, bta-mir-2285ck, bta-mir-2285cl, bta-mir-2285cm, bta-mir-2285cn, bta-mir-2285co, bta-mir-2285cp, bta-mir-2285cq, bta-mir-2285cr-1, bta-mir-2285cr-2, bta-mir-2285cs, bta-mir-2285ct, bta-mir-2285cu, bta-mir-2285cv-1, bta-mir-2285cv-2, bta-mir-2285cw-1, bta-mir-2285cw-2, bta-mir-2285cx, bta-mir-2285cy, bta-mir-2285cz, bta-mir-2285da, bta-mir-2285db, bta-mir-2285dc, bta-mir-2285dd, bta-mir-2285de, bta-mir-2285df, bta-mir-2285dg, bta-mir-2285dh, bta-mir-2285di, bta-mir-2285dj, bta-mir-2285dk, bta-mir-2285dl-1, bta-mir-2285dl-2, bta-mir-2285dm
Treatment with anti-miR-208 prevented weight gain in aging mice, which was due to a reduction in fat weight (69). [score:1]
Similarly, human miR-208 has been shown to have an important role in modulating cardiac function and remo deling (68), and is currently in preclinical trials. [score:1]
[1 to 20 of 2 sentences]
92
[+] score: 2
Together with microRNA-208a, these microRNAs are encoded by introns of myosin genes (MYH6, MYH7, MYH7b). [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]
[1 to 20 of 2 sentences]
93
[+] score: 2
Recent studies have illustrated the participation of miRNAs in the post-transcriptional regulation of WNT/β-catenin pathway, such as miRNA-720, miRNA-141 and miRNA-208a [21]. [score:2]
[1 to 20 of 1 sentences]
94
[+] score: 2
For example, Fichtlscherer et al. [25] performed miRNAs arrays for serum or plasma of controls and CAD patients, and found that cardiac muscle-enriched miRNAs (miR-133 and miR-208a) were overexpressed in patients as compared with controls. [score:2]
[1 to 20 of 1 sentences]
95
[+] score: 1
Levels of miR-208, miR-208b and miR-499 were higher in human endomyocardial samples of DCM patients than in controls. [score:1]
[1 to 20 of 1 sentences]
96
[+] 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]
97
[+] score: 1
173 (miR-186-5p, miR-208a-5p, miR-291a-3p, miR-294-3p, miR-295-3p, miR-302a-3p, miR-302b-3p, miR-302c-3p and miR-302d-3p). [score:1]
[1 to 20 of 1 sentences]
98
[+] score: 1
Bostjancic E, Jerse M, Glavac D, Zidar N: miR-1, miR-133a/b, and miR-208a in human fetal hearts correlate to the apoptotic and proliferation markers. [score:1]
[1 to 20 of 1 sentences]
99
[+] score: 1
It has also been observed that several miRNAs such as- miR-208, miR-381 and miR-339 exhibit significant differences by age. [score:1]
[1 to 20 of 1 sentences]
100
[+] 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]
[1 to 20 of 1 sentences]