MicroRNA-186-5p is expressed highly in ethanol-induced cardiomyocytes and regulates apoptosis via the target gene XIAP

Ethanol has a toxic effect on the heart, resulting in cardiomyocyte damage. Long-term high intake of ethanol leads to a non-ischemic dilated cardiomyopathy termed alcoholic cardiomyopathy (ACM). However, the pathogenesis of alcoholic cardiomyopathy remains unclear. The apoptosis of cardiomyocytes serves an important role in the pathogenesis of ACM. X-linked inhibitor of apoptosis protein (XIAP) is an important anti-apoptotic protein in human tissue cells. To the best of our knowledge, no studies have reported on its function in ethanol-induced cardiomyopathy. Previous works have screened the ACM-associated differentially expressed microRNAs (miRs), including miR-186-5p and miR-488-3p. TargetScan bioinformatics software was used to predict 949 target genes associated with miR-186-5p, and XIAP was demonstrated to be a target of miR-186-5p. The present study firstly analyzed the levels of apoptosis in ethanol-treated cardiomyocytes using flow cytometry. Alterations in the expression levels of miR-186-5p and XIAP were subsequently evaluated in ethanol-treated AC16 cardiomyocytes to assess the specific molecular mechanisms of ethanol-induced cardiomyocyte apoptosis. The levels of apoptosis in AC16 cardiomyocytes increased following ethanol treatment, and further increased with the rise in concentration and action time of ethanol. The expression levels of miR-186-5p were upregulated, and the expression levels of XIAP were downregulated in ethanol-treated cardiomyocytes. miR-186-5p may regulate ethanol-induced apoptosis in cardiomyocytes using XIAP as the direct target gene. This study provides a novel therapeutic target for the prevention and treatment of ACM.