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81 publications mentioning mmu-mir-208a

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

[+] score: 305
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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[+] score: 121
Other miRNAs from this paper: mmu-mir-494
Given that microRNAs can upregulate gene expression by binding to the promoter regions and target sites in the mRNA or indirectly by downregulating repressors [27– 29], we scanned the Bax promoter regions and mRNA for any miR-208a binding sites. [score:12]
A closer inspection of the dysregulated genes showed that miR-208a tended to downregulate genes favoring the extrinsic apoptosis pathway, while upregulating those that favor the intrinsic pathway of apoptosis. [score:8]
Studies have shown that miR-208a functions via upregulation of endoglin to increase myocardial fibrosis, and its silencing downregulates endoglin and reduces type 1 collagen synthesis [31, 32]. [score:7]
We report that miR-208a upregulation alters apoptosis genes' expression and promotes cardiomyocyte apoptosis, while its silencing attenuates apoptosis and improves cardiac function after MI. [score:6]
We found that 0.4 nmol/mL of miR-208a antagomir significantly downregulated miR-208a expression in cultured cardiomyocytes (Figure 1(a)). [score:6]
To silence miR-208a, 300 nmols of miR-208a antagomir per mouse was administered after MI, and this significantly downregulated miR-208a expression at 28 days after MI (Figure 1(c)). [score:6]
Similarly, miR-208a agomir upregulated miR-208a expression in neonatal cardiomyocytes 48 hours after transfection (Figure 1(b)). [score:6]
We believe that this will provide a basis for development of therapies targeting miR-208a in MI. [score:4]
Simulated ischemia of neonatal cardiomyocytes following transfection with miR-208a agomir or antagomir showed that miR-208a upregulation significantly increases apoptosis while its silencing blunts apoptosis during ischemia (Figures 2(a) and 2(b)). [score:4]
miR-208a is a cardiac specific microRNA coded for in an intron of myosin heavy chain 6 (Myh6) gene and regulates cardiac conduction, stress response, and gene expression [6– 9]. [score:4]
In MI, Bax was also shown to be downregulated by miR-208a silencing and may thus be playing a role in miR-208a mediated myocyte apoptosis during ischemia. [score:4]
3.1. miR-208a Antagomir and Agomir Are Effective in Silencing or Upregulating miR-208a, Respectively. [score:4]
Results revealed no predicted miR-208a binding sites both in the gene promoter regions and in mRNA, suggesting that miR-208a may be acting indirectly to alter Bax expression. [score:4]
Bax siRNA attenuated the proapoptotic effect of miR-208a agomir (Figure 2(c)), suggesting that miR-208a functions to promote apoptosis at least in part by upregulating Bax. [score:4]
Interestingly, some researchers have shown that cardiac miR-208a in human MI is persistently upregulated, with the highest levels observed in patients who died within 24 hours [10]. [score:4]
3.2. miR-208a Alters Apoptosis Genes Expression and Promotes Cardiomyocyte Apoptosis during Ischemia. [score:3]
Expression of miR-208a in vivo and in vitro was analyzed using quantitative RT-PCR. [score:3]
Thus, targeted silencing of miR-208a in human MI may be a potentially viable and beneficial therapeutic option. [score:3]
Similarly, p21 (Waf 1), a target of miR-208a, has also been reported to be both anti- and proapoptosis depending on prevailing conditions [25]. [score:3]
Real-time PCR was carried out with the reagents of a Sybr green I mix (Takara, China) in a 20  µL reaction volume (10  µL Sybr green I mix, 200 mM forward and reverse primer, and 2  µL cDNA template) on an MJ Opticon Monitor chromo4 instrument (Bio-Rad, USA) using the following protocol: 95°C for 20 s; 40 cycles of 95°C for 10 s, 60°C for 20 s, and 70°C for 1 s. Normalization for miR-208a was done using U6 while Bax expression was normalized using GAPDH. [score:2]
Cardiomyocytes were transfected with 0.2 nmols/mL of miR-208a agomir for gain of function or 0.4 nmols/mL of miR-208a antagomir for loss of function, by directly adding the agomir or antagomir formulation to the cell culture medium according to manufacturer's instructions (RiboBio Co. [score:2]
The above results were consistent with previous reports which showed that miR-208a silencing or knockout attenuates cardiac fibrosis and hypertrophy in response to cardiac stress [6, 7]. [score:2]
3.3. miR-208a Silencing Attenuates Apoptosis in MI. [score:1]
Our finding that miR-208a antagomir mitigates ischemia induced apoptosis opens a window for its possible therapeutic application in MI. [score:1]
Our findings only open a window and more studies will be needed to further decipher the mechanisms involved in miR-208a mediated apoptosis. [score:1]
RNA was isolated from cultured control or miR-208a agomir transfected cardiomyocytes, 72 hours after transfection. [score:1]
Moreover, miR-208a antagomir also decreased percentage fibrosis at day 28 (Figures 5(c), 5(d), and 5(e)). [score:1]
Myocytes were also analyzed for miR-208a levels after culturing. [score:1]
To gain insight into the effect of miR-208a on apoptosis related genes, we employed custom-built microarrays (RiboBio Co. [score:1]
To assess if therapeutic silencing of miR-208a improves cardiac function in MI, 2-dimensional transthoracic echocardiography studies were performed on 4-5 mice from each group, lightly anesthetized with pentobarbital sodium (25 mg/kg), on days 7 and 28, using a GE Voluson ultrasound system equipped with an 11.5 MHZ high frequency probe. [score:1]
Starting within 2 hours after MI, each antagomir group mouse received a total of 300 nmols of miR-208a antagomir given over 3 consecutive days (days 0, 1, and 2) using 0.2 mLs of normal saline as vehicle, by low pressure tail vein injection, while control and sham group mice each received 0.2 mLs of vehicle only by the same method over the same period of time. [score:1]
Therapeutic Silencing of miR-208a Improves Cardiac Function after MI. [score:1]
Aiming to see any beneficial effects of long term silencing of miR-208a on cardiac function after MI, mice received a total of 300 nmols of miR-208a antagomir, and echo was done at 7 and 28 days. [score:1]
Here we reveal for the first time that miR-208a promotes myocyte apoptosis during ischemia and further show that therapeutic administration of miR-208a antagomir attenuates cardiomyocyte apoptosis, hypertrophy, and fibrosis, coupled with improvement in cardiac function after MI. [score:1]
Although miR-208a has been shown to be proproliferative under certain conditions, we demonstrated that it is proapoptotic in the ischemic setting [22, 23]. [score:1]
qPCR showed that miR-208a silencing in MI also decreased Bax levels at 28 days (Figure 4(d)). [score:1]
The observed decrease in fibrosis provides yet another possible mechanism by which miR-208a antagomir may contribute to improving cardiac function after MI. [score:1]
To the best of our knowledge, our study is the first to demonstrate that antagomir based miR-208a silencing can attenuate cardiomyocyte apoptosis during ischemia and improve cardiac function after MI. [score:1]
3.4. miR-208a Silencing Attenuates Myocyte Hypertrophy and Cardiac Fibrosis in MI. [score:1]
Using 2D echocardiography, we demonstrated improved cardiac function at 28 days after MI in animals therapeutically treated with miR-208a antagomir. [score:1]
To the best of our knowledge, our study is the first to explore the antiapoptotic effects of miR-208a silencing and the therapeutic benefits of miR-208a antagomir in myocardial infarction. [score:1]
To decipher if Bax was essential for miR-208a induced apoptosis, we used siRNA to silence Bax gene. [score:1]
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[+] score: 80
In ZDF-M, cardiac miR-208a expression was higher than that in ZL-M, yet lower than ZL-F and ZDF-F. Moreover, in ZDF-M cardiac Agtr2 expression was similar to ZL-M. Conversely, in ZDF-F, cardiac miR-208a expression was increased while Agtr2 expression was reduced. [score:9]
However, Med13 expression was the highest in ZL-F, indicating that cardiac Med13 mRNA expression in healthy ZL-F could be regulated by mechanisms independent of miR-208a. [score:6]
However, reduction in cardiac Agtr2 expression in ZDF-F in the presence of the highest expression of pro-hypertrophic miR-208a may have contributed to the increased myocardial structural damage observed in ZDF-F rat. [score:5]
Notably, though ZL-F has higher cardiac expression of pro-hypertrophic miR-208a, they also have higher expression of cardio-reparative Agtr2 that may counteract miR-208a’s cardio-detrimental effect and keep the heart healthy. [score:5]
Since increased expression of miR-208a is associated with cardiac hypertrophy, the female-specific increase in cardiac miR-208a expression could have contributed to the increased susceptibility to cardiac hypertrophy in ZDF-F. Increases in the circulating levels of miR-29 family miRNAs in children with T1DM and adults with T2DM 42, 43 emphasize the clinical relevance of this biomarker in DM. [score:5]
Our observations underscore the need for clinically expanding existing cardiac assessments in diabetic female patients to detect myocardial deformation, cardiac hypertrophy and capillary density via non-invasive imaging, as well as suggest miR-208a and AT2R as potential therapeutic targets for cardiac disease in females. [score:5]
DM -associated dysregulation of miR-208a-MED13 signaling and increase in miR-29 family miRNAs occur in both male and female ZDF rats, however, only ZDF-F rats exhibited myocardial damage indicating that cardiac repair is impaired in ZDF-F. It is conceivable that the higher expression of cardio-reparative Agtr2 in ZL-F compared to ZL-M (Fig.   9a) could have provided increased protection despite the higher expression of pro-hypertrophic miR-208a in ZL-F heart compared to ZL-M heart. [score:4]
MED13 is a target of miR-208a, a microRNA that promotes cardiac hypertrophy and heart failure 38– 41. [score:3]
TaqMan MicroRNA Assays (Life Technologies) primers for miR-208a, miR-29a, b, c, and U6 snRNA were used for miRNA targets, and Med13 and 18 S rRNA for mRNA targets. [score:3]
Figure 9Expression patterns of cardioprotective Agtr2 and Med13, and cardio- deleterious miR-208a and diabetic marker miR-29 family miRNAs in heart tissues of 5-month old healthy and diabetic, male and female rats. [score:3]
Though reduction in capillary density was a common phenomenon in both ZDF-F and ZDF-M, this effect is likely more deleterious for the hypertrophied myocardium of ZDF-F. It is conceivable that cardiac hypertrophy, capillary rarefaction, and a female-specific loss of cardio-reparative Agtr2 in the setting of a very high expression of pro-hypertrophic miR-208a could have contributed to increased myocardial structural damage in the form of cardiomyocyte loss and scarring as shown in Fig.   8f. [score:3]
Since ZDF-F exhibited cardiac hypertrophy, we examined whether there was a sex bias in the expression of cardiac miR-208a. [score:3]
Female specific increased expression of cardiac miR-208a (as shown in Fig.   9) could render ZDF-F rats more susceptible to hypertrophy. [score:3]
Cardiac expression of AT2R (Agtr2), Med13, miR-208a, and miR-29 family miRNAs were determined using mRNA and miRNA isolated from frozen heart tissues as described previously [44]. [score:3]
Therefore, miR-208a and AT2R can be potential therapeutic targets for CVD in diabetic females. [score:3]
Thus, T2DM caused an imbalance in cardiac miR-208a- Agtr2 expression pattern that would exacerbate cardiac damage. [score:3]
Elevated miR-208a reduces MED13 expression, thus contributing to obesity 38, 39. [score:3]
Elevated levels of cardiac miR-208a expression in ZL-F and ZDF-F compared to ZL-M and ZDF-M could render female rats more susceptible to cardiac hypertrophy. [score:2]
Cardiac miR-208a expression was elevated in both ZDF-F and ZDF-M compared to lean controls, indicating a diabetes -associated elevation of cardiac miR-208a. [score:2]
The miR-208a expression was higher in both ZL-F and ZDF-F compared to their male counterparts. [score:2]
Interestingly, cardiac expression of miR-208a was higher in ZL-F compared to ZL-M and was the highest in ZDF-F (Fig.   9c, p < 0.05). [score:2]
Thus miR-208a exhibits sex bias. [score:1]
MicroRNA miR-208a promotes cardiac hypertrophy and heart failure 40, 41. [score:1]
MED13-miR-208a-axis differs between male and female diabetic animals. [score:1]
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[+] score: 77
Our results showed that high dose doxorubicin upregulated miR-208a at 7 days, while antagomir was effective in silencing miR-208a upregulation. [score:7]
At 7 days, miR-208a expression was significantly upregulated by doxorubicin treatment. [score:6]
Among the proven targets of miR-208a is GATA4, a cardiac enriched transcription factor whose downregulation following doxorubicin treatment is associated with increased cardiomyocyte apoptosis and heart dysfunction [15– 18]. [score:6]
Among the proven targets of miR-208a is GATA4, a cardiac enriched transcription factor known to regulate the expression of several cardiac genes including the antiapoptotic gene BCL-2 [15– 17]. [score:6]
Consequently, doxorubicin treatment significantly downregulated GATA4 gene expression, while pretreatment with miR-208a antagomir rescued GATA4 levels (Figure 1(b)). [score:6]
Expression of miR-208a, a heart specific microRNA playing a central role in cardiac stress response and known to target GATA4, was analyzed using quantitative RT-PCR. [score:5]
We thus suppose that miR-208a antagomir functions to decreased doxorubicin induced apoptosis at least in part by downregulating miR-208a and hence salvaging GATA4. [score:4]
3.1. miR-208a Is Upregulated by Doxorubicin and Its Silencing Attenuates Doxorubicin Induced Cardiomyocyte Apoptosis. [score:4]
Taken together, we show that doxorubicin upregulates miR-208a and promotes cardiomyocyte apoptosis, while therapeutic silencing of miR-208a attenuates doxorubicin induced myocyte apoptosis with subsequent improvement in cardiac function. [score:4]
However, therapeutic administration of miR-208a antagomir effectively attenuated doxorubicin induced miR-208a upregulation (Figure 1(a)). [score:4]
These findings, which we believe are novel, open a window for new modalities of preventing the cardiotoxic effects of doxorubicin by targeting miR-208a. [score:3]
Our results, which we believe are novel, highlight the therapeutic potential of targeting miR-208a to prevent doxorubicin cardiotoxicity. [score:3]
Thus, having already shown that miR-208a silencing could salvage GATA4, we analyzed BCL-2 gene expression and found that antagomir treated animals had higher BCL-2 levels than controls following doxorubicin treatment (Figure 1(c)). [score:3]
In this study, we report a novel approach of attenuating doxorubicin induced cardiac toxicity by silencing miR-208a, a heart specific microRNA known to target GATA4. [score:3]
miR-208a is a cardiac specific microRNA which regulates cardiac stress responses [20– 23]. [score:2]
Our results showed that antagomir based silencing of miR-208a mitigated doxorubicin induced apoptosis and cardiac dysfunction. [score:1]
Four days before doxorubicin treatment (day −4), antagomir group mice received 50 nmol of miR-208a antagomir each (RiboBio Co. [score:1]
In the current study, we hypothesized that silencing of miR-208a could salvage GATA4 and attenuate doxorubicin induced myocyte apoptosis. [score:1]
To asses if therapeutic silencing of miR-208a attenuates cardiac dysfunction in acute doxorubicin toxicity, animals were lightly anesthetized with pentobarbital sodium (25 mg/kg) on day 7, and two-dimensional transthoracic echocardiography studies performed using Vevo 770 (VisualSonics) ultrasound machine equipped with a 30 MHz cardiac transducer. [score:1]
In addition, 2D echocardiography showed that miR-208a antagomir treated animals had a higher cardiac function than controls 7 days after doxorubicin treatment. [score:1]
To see if miR-208a improves cardiac function, we pretreated mice with 50 nmol of miR-208a antagomir 4 days prior to doxorubicin injection. [score:1]
Our results showed that doxorubicin significantly increased cardiomyocyte apoptosis, while pretreatment of mice with miR-208a antagomir attenuated doxorubicin induced apoptosis (Figures 1(d) and 1(e)). [score:1]
miR-208a is a heart specific microRNA which plays a central role in cardiac stress response [13, 14]. [score:1]
We thus hypothesized that therapeutic silencing of miR-208a may as well salvage GATA4 and protect against doxorubicin induced cardiac toxicity and dysfunction. [score:1]
Therapeutic Silencing of miR-208a Improves Cardiac Function following Doxorubicin Treatment. [score:1]
Given that miR-208a silencing salvaged GATA4, a factor known to decrease doxorubicin induced apoptosis, we analyzed heart sections from the different study groups to see if miR-208a silencing could attenuate doxorubicin induced myocyte apoptosis. [score:1]
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[+] score: 55
Our findings indicate that (i) loss of Nrf2 in the heart results in a modest downregulation of transcripts involved in mitochondrial function, redox homeostasis, metabolism, cardiac pathology, and protein folding, (ii) 27 miRNAs (11 up and 16 downregulated) are significantly altered and differentially regulated in the Nrf2 depleted myocardium, (iii) Nrf2 may either directly or indirectly regulate a sub-set of cardiac miRNAs, and (iv) miR-582-5p, miR-208a-5p, miR-350-3p and miR-30b-5p are likely to contribute to basally downregulated genes in Nrf2 [−/−] hearts. [score:14]
A total of 39 downregulated DEGs contained potential miRNA recognition elements for the following upregulated miRNAs; miR-30b-5p, miR-350-3p, miR-582-5p, and miR-208a-5p. [score:7]
Interestingly, Nrf2 [−/−] hearts displayed 2-fold induction of miR-208a-5p, a well-studied pro-hypertrophic miRNA [48, 49] and we believe this to be a compensatory increase for the downregulation of developmental genes in knockout hearts. [score:6]
In silico target prediction for increased miRNAs suggested that many mRNAs altered in knockout mice may be concurrently regulated by miR-582-5p, miR-208a-5p, miR-350-3p, and miR-30b-5p. [score:5]
Along these lines, we observed an approximate 2-fold (p < 0.01) increase in the expression of miR-208a-5p in the knockout myocardium (Fig. 5c). [score:4]
High throughput data were integrated using prediction algorithms, and these in silico analyses discovered potential recognition elements within 39 repressed mRNAs which matched the seed sequence for 4 upregulated miRNAs; miR-30b-5p, miR-208a-5p, miR-350-3p, and miR-582-5p. [score:4]
Upon stress, miR-208a dictates β -MHC transcription, thereby promoting hypertrophy and cardiogenic gene expression [48, 49]. [score:3]
Using this approach, we discovered 39 transcripts potentially targeted by miR-30b-5p, miR-350-3p, miR-582-5p, and miR-208a-5p. [score:3]
Encoded within the α- MHC gene, miR-208a directly regulates Myh7b and its intronic miRNA, miR-499 in the adult mouse heart. [score:3]
Therefore, rather than serving as indices for pathology, miR-208a-5p and miR-350-3p expression increases in Nrf2 [−/−] mice may reflect susceptibility to adverse cardiac remo deling. [score:3]
In addition to miR-208a, miR-350 has been shown to be an inducer of hypertrophy [50] and was found to be increased by nearly 2-fold (p < 0.05) in Nrf2 [−/−] hearts (Fig. 4c). [score:1]
To support this notion, a 3-fold increase in miR-208a is required for pathological cardiac remo deling [48]. [score:1]
Expression changes were validated for 12 miRNAs using specific primer assays in real-time and revealed a significant decrease in miR-10b-5p, miR-674-3p, miR-3535, and miR-378c while miR-30b-5p, miR-208a-5p, miR-350-3p, and miR-582-5p, and miR-1249-3p levels were increased. [score:1]
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[+] score: 47
Other miRNAs from this paper: mmu-mir-16-1, mmu-mir-16-2, mmu-mir-208b
Hence, the cardiac hyperaldosteronism inhibits miR-208a expression, allowing a sustained Sox6 expression, which in turn inhibits the Myh7 transcription. [score:9]
MiR-208a inhibits the Sox6 factor, which inhibits the expression of both β-MyHC and miR-208b [11], [12]. [score:7]
Moreover, this work reveals an original aldosterone -dependent inhibition of miR-208a in hypertension, resulting in the inhibition of β-myosin heavy chain expression through the induction of its transcriptional repressor Sox6. [score:7]
In rodent heart, alpha-Myosin Heavy Chain (MyHC) and its micro -RNA miR-208a regulate the expression of beta-MyHC and of its intronic miR-208b. [score:4]
0038197.g005 Figure 5(A): scheme of the interplay of miR-208a and -208b on the regulation of Myh7 expression in hypertensive heart, as drawn from literature data. [score:4]
Furthermore, in AS-Ren mice the expression profiles of miR-208a, Sox6, miR-208b (Figure 5 A, C and B) and of β-MyHC (Figure 2D) were reversed by eplerenone (+250%, −50%, +221%, +242%, respectively, vs. [score:3]
Indeed, the maintained expression of miR-208a and the strong induction of miR-208b mRNA in Ren mice (Figure 5B and C) was in agreement with the low Sox6 mRNA level (−50%, p0.05 vs. [score:3]
The specific inhibition of miR-208a observed in AS-Ren mice (−58% vs. [score:3]
Effect of combined cardiac aldosterone and hypertension on cardiac miR-208 and Sox6 expression. [score:3]
As outlined in the section and in Figure 5A, the expression of Myh7 is controlled by miR-208a and the Sox6 transcription factor [11], [12]. [score:3]
The Myh6 gene encodes α-MyHC and the intronic miR-208a. [score:1]
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[+] score: 38
A dual-detargeted virus named vMC [24]-NC, with miR-124 targets in the 5′ NCR and miR-133 plus miR-208 targets in the 3′ NCR, showed the suppression of replication in both nervous and cardiac tissues but retained full oncolytic potency when administered by intratumoral (10 [6] 50% tissue culture infectious doses [TCID [50]]) or intravenous (10 [7] to 10 [8] TCID [50]) injection into BALB/c mice bearing MPC-11 plasmacytomas. [score:9]
In vivo toxicity testing confirmed that miR-124 targets within the 5′ NCR suppressed virus replication in the central nervous system while miR-133 and miR-208 targets in the 3′ NCR suppressed viral replication in cardiac tissue. [score:9]
Therefore, we generated detargeted viruses by inserting two tandem copies of miR-124, miR-125b, or either miR-142-3p target sequences immediately preceding the pCT in the 5′ NCR or two copies each of miR-133b and miR-208a [133/208(2×)] target sequences or four copies of miR-142-3p target sequences in the 3′ NCR of vMC [24]. [score:9]
To enhance its safety profile, microRNA target sequences complementary to miR-124 or miR-125 (enriched in nervous tissue), miR-133 and miR-208 (enriched in cardiac tissue), or miR-142 (control; enriched in hematopoietic tissues) were inserted into the vMC [24] NCRs. [score:3]
This inhibition of viral replication by the 3′ NCR insertions may be due to the presence of miR-142, miR-133, or miR-208 in certain cells or nonspecific effects of the insertions themselves. [score:3]
Unexpectedly, mice injected with vMC [24]-H2 or vMC [24]-C also had reduced mean viral loads in all three tissues, suggesting that either the placement of the insert can control viral replication in vivo or that there are low to intermediate levels of miR-142, miR-133, or miR-208 present regulating viral tropism. [score:2]
Sequences complementary to miR-142, miR-124, miR-125, miR-133, and miR-208 were successfully incorporated (individually or in combination) into the 5′ and 3′ NCRs of the vMC [24] genome. [score:1]
Callis TE, Pandya K, Seok HY, Tang RH, Tatsuguchi M, Huang ZP, Chen JF, Deng Z, Gunn B, Shumate J, Willis MS, Selzman CH, Wang DZ 2009 MicroRNA-208a is a regulator of cardiac hypertrophy and conduction in mice. [score:1]
Additionally, miR-133b and miR-208a are enriched within cardiomyocytes of adult mice and humans (29, 34 – 36). [score:1]
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[+] score: 29
However, our data suggest that in the presence of high levels of T3, the effect of miR-208a on the efficiency of T3-regulated gene expression and pathological signaling is minimal, since it does not prevent T3 -induced gene expression nor does it result in a pathological phenotype under this condition. [score:6]
Increased miR-208a expression is, therefore, expected to decrease T3 action, because Thrap1 expression will be decreased. [score:5]
As already mentioned in the Section “,” expression of miR-208a has been implicated in the development of pathological hypertrophy. [score:4]
The expression pattern of miR-208a (C) and miR-208b (D) in these conditions is similar to the pattern of their host genes. [score:3]
Mir-208a targets the Thyroid Hormone Receptor Associated Protein 1 (Thrap1) (26, 27, 70), which is a component of the TH-receptor/co-factor complex that mediates transcriptional regulation of T3 -dependent genes (26, 27, 71, 72). [score:3]
Furthermore, forced expression of miR-208a induces pathological remo deling (27), whereas blocking of miR-208a attenuates hypertension -induced cardiac dysfunction (28). [score:3]
Both miR-208a and 208b followed the expression of their corresponding host genes Myh6 and Myh7, respectively (Figures 1C,D). [score:3]
For example, miR-208a is required for overload -induced pathological remo deling, including cardiomyocyte hypertrophy, Myh isoform switching, and fibrosis (26, 27). [score:1]
MiRNA-208a and miRNA-208b are triggered in thyroid hormone -induced cardiac hypertrophy - role of type 1 angiotensin II receptor (AT1R) on miRNA-208a/α-MHC modulation. [score:1]
[1 to 20 of 9 sentences]
[+] 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]
[1 to 20 of 8 sentences]
[+] score: 25
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-20a, hsa-mir-22, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-98, hsa-mir-101-1, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-15b, mmu-mir-101a, mmu-mir-126a, mmu-mir-130a, mmu-mir-133a-1, mmu-mir-142a, mmu-mir-181a-2, mmu-mir-194-1, hsa-mir-208a, hsa-mir-30c-2, mmu-mir-122, mmu-mir-143, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-181a-1, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-15b, hsa-mir-122, hsa-mir-130a, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-142, hsa-mir-143, hsa-mir-126, hsa-mir-194-1, mmu-mir-30c-1, mmu-mir-30c-2, mmu-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: 20
For example, miR-208, miR-9, let-7a, 7b, and miR-22* were found to be up-regulated in transformed IEC-6 cells, whereas miR-539, miR-181d, and miR-146a were down-regulated. [score:7]
Consistent with the specific expression of MHC in the heart and the pulmonary myocardium, miR-208 is expressed specifically in the heart and at trace levels in the lung [33]. [score:5]
Among these differentially expressed miRNAs, we verified the alteration of miR-208 and miR-22*. [score:3]
So the expression of miR208 and miR22* was chosen to be validated. [score:3]
miR-208 is encoded by intron 27 of the human and mouse MHC gene. [score:1]
The relationship between miR-208 and tumorigenesis was not clear and needed further study. [score:1]
[1 to 20 of 6 sentences]
[+] score: 19
Other miRNAs from this paper: mmu-mir-499, dre-mir-499, mmu-mir-208b
The increased transcription of Myh6 and Myh7 in Sox6 KO muscle, therefore, could lead to upregulation of miR-208, which in turn, suppress fast fiber specific gene expression. [score:8]
It has been reported that miR-208 suppresses expression of THRAP1, which promotes fast fiber specific gene expression [96]. [score:7]
It should be noted that miR-208, along with miR-499, also targets the 3'-UTR region of Sox6 [68, 97, 98]. [score:3]
In the intron sequences of Myh6 and Myh7, miR-208a and miR-208b are encoded, respectively [95]. [score:1]
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[+] score: 17
IPost up-regulated miR-1, miR-15b, miR-21, miR-24, miR-26a, miR-27, miR-133a, miR-199a, miR-214, miR-208 and miR-499, while down-regulated miR-23a and miR-9 as compared with Sham group. [score:6]
Compared with sham group, the expressions of miR-1, miR-15b, miR-21, miR-24, miR-26a, miR-27, miR-133a, miR-199a, miR-214, miR-208 and miR-499 were increased in IPost hearts, while miR-9 and miR-23a were down-regulated in IPost mo dels. [score:5]
Then real-time quantitative PCR was performed to quantify the expression level of miR-1, miR-9, miR-15b, miR-21, miR-23a, miR-24, miR-26a, miR-27, miR-133a, miR-199a, miR-208, miR-214 and miR-499 with SYBR Green PCR Master Mix (Applied Biosystems) according to the manufacturer’s instructions. [score:3]
As previously reported, a collection of miRNAs were abnormally expressed in ischemic mouse hearts in response to I/R injury, such as miR-1, miR-9, miR-15b, miR-21, miR-23a, miR-24, miR-26a, miR-27, miR-133a, miR-199a, miR-208, miR-214 and miR-499 [20, 21, 28]. [score:3]
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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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[+] score: 14
In the present study, miR-208a was upregulated in P19 cells exposed to PCBs, and could therefore have a role in the development of heart disease caused by PCB exposure. [score:7]
The expression level of miR-208a has been demonstrated to gradually increase during mouse heart development. [score:4]
Transgenic overexpression of miR-208a was sufficient to induce hypertrophic growth in the mouse heart [9]. [score:3]
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[+] score: 13
It has been shown that miRNAs are determinants of the physiology and pathophysiology of the cardiovascular system and altered expression of muscle- and/or cardiac-specific miRNAs such as the miRNAs named miR-1, miR-208 and miR-133 in myocardial tissue is involved in heart development and cardiovascular diseases, including myocardial hypertrophy, heart failure and fibrosis [11– 14]. [score:6]
Although, this study focus in the acute phase of the experimental Chagas disease some miRNAs (miR-133, miR-208) were found down regulated at 45 dpi in accordance with previously reported in human heart of Chagas chronic patients [15]. [score:4]
In the study, we have found that the same muscle- and/or cardiac-specific miRNAs, miR-1, miR-133 and miR-208 were downregulated in CCC myocardium as compared to control myocardium [15]. [score:3]
[1 to 20 of 3 sentences]
[+] score: 12
To further explore this aspect and discard the possibility of eventual contamination of our samples with differentiated cardiomyocytes, we independently determined the expression levels of miR-1, a hallmark of cardiomyocyte differentiation, and two additional miRs known to be essential for muscle differentiation processes: miR-208a and miR-206. [score:3]
In contrast, the expression levels of mir-208a are very similar in both cell types and heart tissue, albeit undetectable in BMCs, confirming the commitment of CSCs to the cardiomyocyte lineage. [score:3]
The parallel identification of miR-208 expression, an intronic miR encoded in the cardiac alfa-myosin heavy chain (αMHC) gene, which promotes the transition from the embryonic to adult isoforms of cardiac contractile proteins, further stresses the CSC commitment to the adult cardiomyocyte lineage. [score:3]
The expression of miR-133a, miR-133b and miR-208 is considered a specific mark of cardiomyocyte lineage differentiation [13]– [16]. [score:2]
miR-208a is encoded in an intron of the myosin heavy chain gene Myh6 [41], [42] and is part of a family of so-called ‘myomirs’, named after their important roles in muscle differentiation. [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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[+] score: 11
Analysis of the expression of cardiomyocyte-specific miRNAs miR-1, miR-133a/b, and miR-208a/b and mRNAs MYH6 and TNNT2 showed upregulation of miR-1, miR-133 a/b, miR-208a/b, and MYH6 and TNNT2 in differentiated cardiomyocyte cells compared to freshly isolated Sca-1 [+]CD31 [−] cells (Figure 6). [score:5]
In our study, mmu-miR-1 was not differently expressed and mmu-miR-133 and mmu-miR-208a expression was reduced in Sca-1 [+]CD31 [−] compared to Sca-1 [+]CD31 [+] cells. [score:4]
Analysis of the expression of cardiomyocyte-specific miRNAs miR-1, miR-133a/b, and miR-208a/b and mRNAs MYH6 and TNNT2 revealed miRNA patterns indicative of stem cell characteristics. [score:1]
Among miRNAs expressed in the heart, miR-1, miR-133, miR-208, and miR-499 are the most commonly investigated subtypes. [score:1]
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[+] score: 10
For example, the MyomiRs miR-208a, -208b and -499 control myosin heavy chain isoform expression [4], miR-133a and miR-1 are crucial regulators of cardiac differentiation and development [1] and miR-195 overexpression is sufficient to induce hypertrophy in mice, while ablation of miR-208a is protective [5]. [score:7]
We also noted that HL-1 cells expressed higher levels of miR-208a than miR-208b, seen as a marker of adult rather than embryonic cardiac tissue [1]. [score:3]
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[+] score: 10
Two further examples are Mir208a and Mir208b, which are located in introns of Myh6 and Myh7 respectively and are differentially expressed in parallel with their host gene expression in mouse heart, suggesting that the miRNAs are processed from the intronic transcript rather than being transcribed as a separate RNA [40,41]. [score:5]
miR-208 knockout mice display a reduced hypertrophic response to thoracic aortic banding, and this microRNA is thought to regulate stress -dependent gene expression in the heart [40] and is required for normal cardiac conduction [41]. [score:5]
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[+] score: 10
Our group has observed dysregulated miRNA expression in heart samples from CCC patients [21] and acute T. cruzi infection in mice [33] including miR-133 and miR-208, which regulate heart genes related to cardiovascular disease 34– 39. [score:7]
Satoh M Minami Y Takahashi Y Tabuchi T Nakamura M Expression of microRNA-208 is associated with adverse clinical outcomes in human dilated cardiomyopathyJ Card Fail. [score:3]
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[+] score: 9
0130658.g006 Fig 6 (A) qPCR validation of selected miRs from the microRNA array showing significant down-regulation of miR-21 and miR-92a and significant up-regulation of miR-27, miR-29, miR-208 and miR-214 in CR compared to Ad lib. [score:6]
In addition, miR-27, miR-29, miR-208 and miR-214 were significantly up-regulated in CR as compared to AL groups (+2.969±0.5318, P<0.05; +7.483±1.084, P<0.002; +2.483±0.9468, P<0.009; and +2.003±0.5865, P<0.02; fold change respectively, N = 3) (Fig 6A). [score:3]
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[+] score: 9
To test whether the observed cardiac or muscle miRNA expression profiles changes are temporal, we compared the miRNA expression profiles of mice hearts at postnatal days 0, 3, 8, and 14 by using qRT-PCR and found miR-1a-3p, miR-133b-3p, miR-208b-3p, and miR-206-3p were significantly decreased while miR-208a-3p was upregulated (Figure 1). [score:7]
An increasing number of miRNAs with different functions in heart development have also been identified, including miR-1, miR-208, miR-133, miR-206, miR-126, miR-143, miR-145, and miR-499; from this group, we analyzed the 7 miRNAs most relevant to postnatal heart growth. [score:2]
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[+] score: 9
Other miRNAs from this paper: rno-mir-208a
We also demonstrated that 12 weeks of Rapamycin treatment in ZO rats resulted in downregulation of cardiac levels of microRNA miR-208a. [score:4]
We have reported previously that Rapamycin treatment suppressed miR-208a that promotes fibrosis in ZO rats [9]. [score:3]
We observed that Rapamycin (750  μg/kg/day; 12 weeks) reduced body weight, body fat, and cardiac microRNA miR-208a (implicated in promoting hypertrophy and fibrosis) and increased cardiac Med13 (that promotes whole body metabolism in Zucker diabetic fatty rats) [9]. [score:1]
miR-208a is a marker for cardiac dysfunction and fibrosis. [score:1]
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[+] score: 8
In recognition that cardiovascular disease and cardiac remo deling is associated with simultaneous dysregulation of several miRNAs (e. g. miR-1, miR-34a, miR-133, miR-199b, miR-320 [11], [15], [36]– [38]) or miRNA families (e. g. miR-34 family [10], miR-208 family [39]), tiny 8-mer seed -targeting LNA-antimiRs could provide an advantage by simultaneous inhibition of entire miRNA seed families [10], [27]. [score:8]
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[+] 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]
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[+] 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]
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[+] 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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[+] score: 6
By contrast, microRNA-208a and microRNA-195 were up-regulated in cardiac hypertrophy, which were sufficient to drive pathological cardiac growth when over-expressed in transgenic mice, respectively [10, 11]. [score:6]
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[+] score: 6
We performed qPCR to detecct the expression levels of ANF, BNP and several stress-responsive miRNAs (miR-29, miR-195 and miR-208) in Myh6-miR-24 transgenic and control hearts. [score:3]
Similarly, miR-29, miR-195 and miR-208 were dramatically reduced upon MI, but were partially restored by overexpression of miR-24 in cardiomyocytes (Fig. 4K). [score:3]
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[+] 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]
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[+] score: 6
Other miRNAs from this paper: mmu-mir-208b
Previously, our study had found that insulin promotes VSMCs proliferation and migration via microRNA-208 -mediated downregulation of p21 and inducing dopamine D [1] receptor dysfunction, and activation of the dopamine D [4] receptor suppresses the effect of insulin on VSMCs [30– 32]. [score:6]
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[+] score: 6
However, for miR-208a the result was closer to the Febit result, which detected an up-regulation (whereas Affymetrix did not). [score:4]
miR-208a was an example for miRNAs which were detected as being regulated only by the Febit platform. [score:2]
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[+] score: 5
We found that Trbp regulates the expression and function of cardiac-specific miR-208a, which represses the transcription factor Sox6. [score:4]
One of the miRNAs that mediates the function of Trbp in the heart is the cardiac-specific miR-208a [23]. [score:1]
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[+] score: 5
Notably, cardiac-specific miR-1, miR-133, miR-208 and miR-499 were all suppressed by two or more orders of magnitude [34], [35], as were the stemness and cell cycle repressors miR-141 and miR-137 [36]; in contrast, the proliferative miRNAs, miR-222 [37], increased dramatically in MDCs, and miR-221 was undetectable in myocytes but highly expressed in MDCs (Figure 5D). [score:5]
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[+] score: 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]
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Specifically, transgenic over expression of miR-208a in the heart has been shown to result in cardiac hypertrophy together with reduced expression of Mstn [19]. [score:5]
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[+] score: 4
Reports have shown that miR-208 and miR-140 affect their host genes 25, 26; however, miR-26 suppresses its host gene to regulate neurogenesis [27]. [score:4]
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[+] score: 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]
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2. Tang Y, Cui Y, Li Z, Jiao Z, Zhang Y, He Y, Chen G, Zhou Q, Wang W, Zhou X, Luo J, Zhang S. Radiation -induced miR-208a increases the proliferation and radioresistance by targeting p21 in human lung cancer cells. [score:3]
MicroRNA-130b PPARγ BCL-2 Apoptosis NSCLC Several microRNAs (miRNAs), such as miR-21, miR-152, miR-148b and miR-208a, play critical roles in lung cancer progression through modulating growth, apoptosis, metastasis and invasion [1– 4]. [score:1]
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[+] score: 4
Several miRNAs are upregulated and associated with tumorigenesis in ESCC, such as miR-21, miR-138, miR-223, miR-92a, miR-9, and mir-208. [score:4]
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[+] score: 4
Targeted deletion of miR-208, while not leading to a developmental defect, blocked the heart's ability to develop a hypertrophic response to stress [16]. [score:4]
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[+] score: 4
qPCR confirmation of exosome-specific expression on miR-10b and miR-208. [score:3]
To validate these data we performed qPCR with pre-amplification cycle for two exosome-specific miRNAs, miR-10b and miR-208. [score:1]
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[+] score: 4
This may reflect the challenge of detecting the early stages of miRNA downregulation, particularly for stable mature miRNAs such as miR-208 that has a half-life of >12 days [28]. [score:4]
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[+] score: 3
In addition to the finding that miRNAs as a whole are essential to proper muscle formation, individual miRNAs have been shown to play key roles in myogenesis, including species that regulate satellite cell quiescence (miR-489, [6]), promote proliferation (miR-133, miR-27 [7, 8]), promote myoblast differentiation (miR-206, miR-1, miR-486 [9– 11]), and regulate fiber type switching (miR-499, miR-208a, miR-208b [12]). [score:3]
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[+] score: 3
Other miRNAs from this paper: mmu-mir-208b
Recent breakthrough data show for the first time that modulation of a single cardiac signaling pathway have profound effects on global energy homeostasis: inhibition of miR-208 in the heart of mice confers resistance to high-fat diet -induced obesity, and improves systemic insulin sensitivity and glucose tolerance [39]. [score:3]
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[+] score: 3
For example, miRNA-21, miRNA-23a, miRNA-24, miRNA-133, miRNA-208/miRNA-195 and miRNA-199 have been shown to be involved in cardiac hypertrophy (15- 17), miRNA-1 in arrhythmia (18), miRNA-29 and miRNA-21 in cardiac fibrosis (19, 20), miRNA-210 and miRNA-494 in ischemic heart disease (21) and miRNA-129 in heart failure (22). [score:3]
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[+] score: 3
Highly expressed miRNAs in skeletal muscle tissue are termed myomiRs, which include miR-1, miR-133a, miR133-b, miR-206, miR-208, miR208b, miR486, and miR-499 (Van Rooij et al., 2008). [score:3]
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[+] score: 3
Other specifically expressed miRNAs that we verified are mir-208, which is known to be restricted to the heart [47] and mir-122, the most prominent miRNA in liver [48]. [score:3]
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[+] score: 3
Other miRNAs from this paper: rno-mir-208a, rno-mir-499, mmu-mir-499
Transgenic expression of miR-499 also effectively reduced the elevated Sox6 mRNA level in miR-208a [-/-] hearts and reduced the Sox6 mRNA level in skeletal muscles of MCK-miR-499 transgenic mice [19]. [score:3]
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[+] score: 3
Other miRNAs from this paper: mmu-mir-499
Normalization of Myh7 levels is associated with improved cardiac function and survival in rodent mo dels of heart failure in which the microRNA miR-208a has been targeted [36, 37]. [score:3]
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[+] 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]
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[+] score: 3
For instance, miR-208a conditional knockout mice display little to no effect on cardiovascular development or normal function, but show significantly reduced stress-responsive cardiac hypertrophy in response to pressure overload [53]. [score:3]
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[+] score: 3
However, the expression of both OVOL TFs resulted in the induction of miR-429, miR-208 and miR-200c. [score:3]
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[+] 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]
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[+] score: 2
Xiao et al demonstrated that serum miR-208a and miR-499 were elevated after AMI and might be potential biomarkers for AMI [47]. [score:1]
Circ Cardiovasc Genet [Epub ahead of print] 47 Xiao J, Shen B, Li J, Lv D, Zhao Y, et al (2014) Serum microRNA-499 and microRNA-208a as biomarkers of acute myocardial infarction. [score:1]
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[+] score: 2
Other miRNAs from this paper: mmu-mir-23a
Huang Y. Yang Y. He Y. Huang C. Meng X. Li J. MicroRNA-208a Potentiates Angiotensin II-triggered Cardiac Myoblasts Apoptosis via Inhibiting Nemo-like Kinase (NLK) Curr. [score:2]
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[+] score: 2
Knockdown of miR-208a helps to attenuate apoptosis and improve cardiac function after myocardial infarction (11). [score:2]
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[+] score: 2
Other miRNAs from this paper: mmu-mir-328, mmu-mir-223, mmu-mir-208b, mmu-mir-664
MicroRNA-208a is a regulator of cardiac hypertrophy and conduction in mice. [score:1]
miR-208. [score:1]
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[+] score: 2
The specificity of the RT-qPCR assay was further supported by the biodistribution patterns obtained for the tissue-specific miRNAs miR-122 (liver), miR-208a (heart) and miR-124-3p/-5p (brain), and the ubiquitously expressed miRNAs miR-191 and miR-16, using the method (Figure 3a). [score:2]
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[+] 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]
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[+] score: 2
Li H Zheng D Zhang B Liu L Ou J Chen W Xiong S Gu Y Yang J Mir-208 promotes cell proliferation by repressing SOX6 expression in human esophageal squamous cell carcinomaJ Transl Med. [score:2]
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[+] score: 2
In addition, recent studies have implicated regulation of several microRNAs (miRNAs) in hypertrophy, including miR-1, miR-133, and miR-208 [11], [12], [13]. [score:2]
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[+] score: 2
In our obese animal mo del, cardiac hypertrophy is present in spite of miR-499 being down regulated, showing that miR-208a/miR-499 pathway is not the driving force to generate the increase of heart mass and leaving open this possibility to other signal pathways like IGF-1, TGF-β or inflammatory cytokines related to diabetic cardiomyopathy (Table  1) 48, 49. [score:2]
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[+] 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]
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[+] 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]
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Quantitative miRNA analysis was restricted to cardiomyocyte-enriched miRNAs: miR-1, miR-133a/b, miR-208a/b, and miR-499. [score:1]
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[+] score: 1
Two other important cardiac miRNAs, mir-208a and mir-208b, do not exist in zebrafish. [score:1]
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[+] score: 1
Other miRNAs from this paper: hsa-mir-208a, mmu-mir-208b, hsa-mir-208b
We have shown recently that Neb–induced resistance to weight gain in leptin resistant rats involves the cardiac miR-208-MED13 axis [21]. [score:1]
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[+] score: 1
Among the differentially expressed microRNAs were miR-181a, miR-208-5p or miR-499, miR-130a, miR-26a and miR-30c with previously characterised functions in skeletal muscle. [score:1]
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[+] score: 1
MiRNAs miR-1272, miR-548, miR-208a, miR-1298, miR-708 and miR140-3p were predicted to bind to the CD38 3’UTR with high context score. [score:1]
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[+] score: 1
A group of miRNAs, highly enriched in skeletal muscle (referred to as myomiRs), has recently been identified and includes miR-1, miR-133a, miR-133b, miR-206, miR-208, miR-208b, miR-486, and miR-499 [33– 37]. [score:1]
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Several key microRNAs such as miR-208a, miR-221, and miR-340-5p were identified in failing hearts. [score:1]
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[+] score: 1
MicroRNA-208a is a regulator of cardiac hypertrophy and conduction in mice. [score:1]
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[+] score: 1
Other miRNAs from this paper: hsa-let-7f-1, hsa-let-7f-2, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-32, mmu-mir-1a-1, mmu-mir-133a-1, mmu-mir-134, mmu-mir-135a-1, mmu-mir-144, mmu-mir-181a-2, mmu-mir-24-1, mmu-mir-200b, mmu-mir-206, hsa-mir-208a, mmu-mir-122, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-181a-1, hsa-mir-214, hsa-mir-200b, mmu-mir-299a, mmu-mir-302a, hsa-mir-1-2, hsa-mir-122, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-144, hsa-mir-134, hsa-mir-206, mmu-mir-200a, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-24-2, mmu-mir-328, hsa-mir-200c, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-181b-2, mmu-mir-25, mmu-mir-32, mmu-mir-200c, mmu-mir-181a-1, mmu-mir-214, mmu-mir-135a-2, mmu-mir-181b-1, mmu-mir-181c, hsa-mir-200a, hsa-mir-302a, hsa-mir-299, hsa-mir-361, mmu-mir-361, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-367, hsa-mir-377, mmu-mir-377, hsa-mir-328, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-181b-2, hsa-mir-20b, hsa-mir-429, mmu-mir-429, hsa-mir-483, hsa-mir-486-1, hsa-mir-181d, mmu-mir-483, mmu-mir-486a, mmu-mir-367, mmu-mir-20b, hsa-mir-568, hsa-mir-656, mmu-mir-302b, mmu-mir-302c, mmu-mir-302d, mmu-mir-744, mmu-mir-181d, mmu-mir-568, hsa-mir-892a, hsa-mir-892b, mmu-mir-208b, hsa-mir-744, hsa-mir-208b, mmu-mir-1b, hsa-mir-302e, hsa-mir-302f, hsa-mir-1307, eca-mir-208a, eca-mir-208b, eca-mir-200a, eca-mir-200b, eca-mir-302a, eca-mir-302b, eca-mir-302c, eca-mir-302d, eca-mir-367, eca-mir-429, eca-mir-328, eca-mir-214, eca-mir-200c, eca-mir-24-1, eca-mir-1-1, eca-mir-122, eca-mir-133a, eca-mir-144, eca-mir-25, eca-mir-135a, eca-mir-568, eca-mir-133b, eca-mir-206-2, eca-mir-1-2, eca-let-7f, eca-mir-24-2, eca-mir-134, eca-mir-299, eca-mir-377, eca-mir-656, eca-mir-181a, eca-mir-181b, eca-mir-32, eca-mir-486, eca-mir-181a-2, eca-mir-20b, eca-mir-361, mmu-mir-486b, mmu-mir-299b, hsa-mir-892c, hsa-mir-486-2, eca-mir-9021, eca-mir-1307, eca-mir-744, eca-mir-483, eca-mir-1379, eca-mir-7177b, eca-mir-8908j
For instance, miR-208, miR-302 (a-d), miR-367 were not detected (at >10 cpm on average) in the heart tissue; miR-134 and miR-208a were not detected in skeletal muscles; miR-483 in liver; or miR-483 and miR-377 in bone [36]. [score:1]
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Ji X Plasma miR-208 as a Biomarker of Myocardial InjuryClin. [score:1]
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[+] score: 1
Other miRNAs from this paper: hsa-mir-208a, mmu-mir-208b, hsa-mir-208b
A miR-208-Mef2 axis drives the decompensation of right ventricular function in pulmonary hypertension. [score:1]
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[+] score: 1
In addition, a panel of tissue-specific miRNAs was also identified, including miR-122 (liver), miR-133a (muscle) and miR-208a (heart) [27]. [score:1]
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[+] score: 1
MicroRNA-208a is a regulator of cardiac hypertrophy and conduction in mice. [score:1]
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[+] score: 1
In agreement with prior studies in animal mo dels of heart failure it was found that miR-21 and miR-208b increased both in the infarct area and in the border zone, miR-1 and miR-208a decreased in the infarct area, miR-133a decreased in the border zone whereas the trend decrease in the infarct area did not achieve statistical significance, and miR-133b exhibited only a non-significant diminution both in the infarct and in the border zone [18]– [22] (Figure S5). [score:1]
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