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Here, we determined the role of miR expression in cardiomyocyte apoptosis during hypoxia and reoxygenation. The rat cardiomyocyte cell line H9c2 was incubated for 3\u2009h in normal or hypoxia medium, followed by reoxygenation for 24\u2009h and transfection with a miR\u2010302 mimic or antagomir. The effect of miR\u2010302 on myeloid leukemia cell\u2010differentiation protein\u20101 (Mcl\u20101) expression was determined by western blot, real\u2010time polymerase chain reaction, and luciferase reporter assays, with cell viability assays. We observed that miR\u2010302 expression was elevated by hypoxia\/reoxygenation injury and increased further or decreased by transfection of the miR\u2010302 mimic or miR\u2010302 antagomir, respectively. Additionally, elevated miR\u2010302 levels increased apoptosis\u2010related protein levels and cardiomyocyte apoptosis, and luciferase reporter assays revealed miR\u2010302 binding to the Mcl\u20101 mRNA 3\u2032 untranslated region. Our findings suggested that miR\u2010302 overexpression aggravated hypoxia\/reoxygenation\u2010mediated cardiomyocyte apoptosis by inhibiting antiapoptotic Mcl\u20101 expression, thereby activating proapoptotic molecules. Furthermore, results indicating cardiomyocyte rescue from hypoxia\/reoxygenation injury following treatment with miR\u2010302 antagomir suggested that miR\u2010302 inhibition might constitute a therapeutic strategy for protection against cardiomyocyte apoptosis during hypoxia\/reoxygenation injury.<\/jats:p>","DOI":"10.1155\/2017\/7968905","type":"journal-article","created":{"date-parts":[[2017,4,11]],"date-time":"2017-04-11T21:02:24Z","timestamp":1491944544000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":26,"title":["Inhibition of miR\u2010302 Suppresses Hypoxia\u2010Reoxygenation\u2010Induced H9c2 Cardiomyocyte Death by Regulating Mcl\u20101 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