MiR‐423‐5p inhibition alleviates cardiomyocyte apoptosis and mitochondrial dysfunction caused by hypoxia/reoxygenation through activation of the wnt/β‐catenin signaling pathway via targeting MYBL2

摘要: MicroRNA (miR) plays an integral role in cardiovascular diseases. M-iR-423-5p is aberrantly expressed patients with myocardial infarction and heart failure. The aim of the present study was to roles mechanisms miR-423-5p hypoxia/reoxygenation (H/R) mediated cardiomyocytes injury. H9C2 cells were transfected negative control, mimic, inhibitor for 48 hr, followed by exposed H/R condition. Cell apoptosis rate, caspase 3/7 activities, Bax cleaved-caspase 3 (c-caspase 3) protein levels assayed flow cytometry, Caspase-Glo Assay kit, western blot analysis, respectively. Furthermore, mitochondrial membrane potential, adenosine triphosphate (ATP) content, reactive oxygen species (ROS) production, Drp1 expression also investigated. dual-luciferase reporter assay used evaluate relationship between Myb-related B (MYBL2). wnt/β-catenin assessed analysis. results revealed that triggered expression. Overexpression promoted cardiomyocyte apoptosis, enhanced activities 3/7, upregulated c-caspase 3. upregulation caused loss potential reduction ATP augment ROS production However, opposite trends observed upon suppression miR-423-5p. In addition, could target 3' untranslated region MYBL2. depletion led activation signaling pathway via targeting Knockdown MYBL2 obviously reversed dysfunction. Taken together, reduced H/R-induced injury through cardiomyocytes.