MiR‐134‐5p targeting XIAP modulates oxidative stress and apoptosis in cardiomyocytes under hypoxia/reperfusion‐induced injury

MicroRNA‐134‐5p (MiR‐134‐5p) has been proposed as a promising novel biomarker for the diagnosis of acute myocardial infarction (AMI). However, the biological role of miR‐134‐5p in ischemic cardiomyocytes has been little disclosed yet. Expression of miR‐134‐5p and X‐linked inhibitor of apoptosis protein (XIAP) was detected using RT‐qPCR and western blot. Oxidative stress and cell apoptosis were determined by enzyme‐linked immunosorbent assays, 3‐(4, 5‐dimethylthiazole‐2‐y1)‐2, 5‐biphenyl tetrazolium bromide assay, flow cytometry, western blot, and terminal‐deoxynucleoitidyl transferase‐mediated nick end labeling (TUNEL). The interaction between miR‐134‐5p and XIAP was confirmed by luciferase reporter assay. Expression of miR‐134‐5p was upregulated in serum of AMI patients and hypoxia/reoxygenation (H/R)‐induced cardiomyocytes (AC16 and HCM). MiR‐134‐5p downregulation could inhibit H/R‐mediated release of lactic dehydrogenase enzyme (LDH) and malondialdehyde (MDA), and promote superoxide dismutase (SOD) and glutathione peroxidase (GSH‐PX) levels. Meanwhile, cell viability was increased, while the apoptosis rate and TUNEL positive cells were inhibited by miR‐134‐5p downregulation in H/R‐treated AC16 and HCM cells. Mechanically, XIAP was downregulated and targeted by miR‐134‐5p in H/R‐induced cardiomyocytes in vitro. Overexpression of XIAP inhibited oxidative stress and cell apoptosis in H/R‐treated AC16 and HCM cells, which was similar to miR‐134‐5p knockdown. Moreover, downregulation of XIAP could partially reverse the effect of miR‐134‐5p knockdown in H/R‐induced cardiomyocytes. Knockdown of miR‐134‐5p protected cardiomyocytes from H/R‐induced oxidative stress and apoptosis in vitro through targeting XIAP.