Inhibition of MIR-302 Suppresses Hypoxia-Reoxygenation-Induced H9c2 Cardiomyocyte Death by Regulating Mcl-1 Expression

Yao Ching Fang, Chi Hsiao Yeh

研究成果: 雜誌貢獻文章同行評審

18 引文 斯高帕斯(Scopus)

摘要

MicroRNAs play important roles in cell proliferation, differentiation, and apoptosis, and their expression influences cardiomyocyte apoptosis resulting from ischemia-induced myocardial infarction. 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 h in normal or hypoxia medium, followed by reoxygenation for 24 h and transfection with a miR-302 mimic or antagomir. The effect of miR-302 on myeloid leukemia cell-differentiation protein-1 (Mcl-1) expression was determined by western blot, real-time polymerase chain reaction, and luciferase reporter assays, with cell viability assays. We observed that miR-302 expression was elevated by hypoxia/reoxygenation injury and increased further or decreased by transfection of the miR-302 mimic or miR-302 antagomir, respectively. Additionally, elevated miR-302 levels increased apoptosis-related protein levels and cardiomyocyte apoptosis, and luciferase reporter assays revealed miR-302 binding to the Mcl-1 mRNA 3′ untranslated region. Our findings suggested that miR-302 overexpression aggravated hypoxia/reoxygenation-mediated cardiomyocyte apoptosis by inhibiting antiapoptotic Mcl-1 expression, thereby activating proapoptotic molecules. Furthermore, results indicating cardiomyocyte rescue from hypoxia/reoxygenation injury following treatment with miR-302 antagomir suggested that miR-302 inhibition might constitute a therapeutic strategy for protection against cardiomyocyte apoptosis during hypoxia/reoxygenation injury.
原文英語
文章編號7968905
期刊Oxidative Medicine and Cellular Longevity
2017
DOIs
出版狀態已發佈 - 一月 1 2017
對外發佈

ASJC Scopus subject areas

  • 生物化學
  • 老化
  • 細胞生物學

指紋

深入研究「Inhibition of MIR-302 Suppresses Hypoxia-Reoxygenation-Induced H9c2 Cardiomyocyte Death by Regulating Mcl-1 Expression」主題。共同形成了獨特的指紋。

引用此