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Topics {✒️}

month download article/chapter zi-qin zhao small double-stranded rnas ongoing enterovirus-induced myocarditis microrna-mediated gene regulation myocardial ischemia/reperfusion injury related subjects real-time rt-pcr connexin channel permeability full article pdf cellular biochemistry aims jones-rhoades mw privacy choices/manage cookies muscle-specific microrna muscle specific microrna regulates notch signaling van veen ta real-time pcr cheng-liang luo viral myocarditis published alleviates viral myocarditis hong-mei xu altered microrna expression investigated mir-1 expression skeletal muscle proliferation gap junction channels muscle-specific micrornas yu-jie ding microrna feedback circuit article xu microrna-target recognition mir-1 expression levels tissue-specific expression mammalian microrna targets bei-xu li european economic area ai-min xue midbrain dopamine neurons bartel dp neonatal rat cardiomyocytes evoke cardiac hypertrophy gap junctional connexins specific molecular targets article molecular expression cx43 protein cx43 protein expression conditions privacy policy post-transcriptional repression check access instant access

Questions {❓}

• Cannell IG, Kong YW, Bushell M (2008) How do microRNAs regulate gene expression?

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      description:MicroRNAs (miRNAs) are increasingly reported to have important roles in diverse biological and pathological processes. Changes in abundance of muscle-specific microRNA, miR-1, have been implicated in cardiac disease, including arrhythmia and heart failure. However, the specific molecular targets and cellular mechanisms involved in the miR-1 function in the heart are only beginning to emerge. In this study, we investigated miR-1 expression and its potential role in the mouse model of viral myocarditis (VMC). The expression levels of miR-1 and its target gene Connexin 43 (Cx43) were measured by real-time PCR and western blotting, respectively. The miR-1 expression levels were significantly increased in cardiac myocytes from VMC mice in comparison with control samples (relative expression: 10 ± 2.5 vs. 31 ± 7.6, P < 0.05). Among the target genes of miR-1, the expression Cx43 protein was significantly reduced in such mice while there was no significant difference in the its mRNA levels. Our results revealed an inverse correlation between miR-1 levels and Cx43 protein expression in VMC samples. Using a bioinformatics-based approach, we found two identical potential binding sites were found in mouse miR-1 and Cx43 3′- untranslated region, this confirms a possible regulatory role of miR-1. In cultured, miRNA transfected myocardial cells, we show overexpression of miR-1 accompanied by a decrease in Cx43 protein’s expression. There was only a slight (not statistically significant) drop in Cx43 mRNA levels. Our results indicate that miR-1 is involved in VMC via post-transcriptional repression of Cx43, and might constitute potentially valuable data for the development of a new approach in the treatment of this disease.
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