Investigating the effect of lncRNA HOTAIR on apoptosis induced by myocardial ischemia-reperfusion injury

The present study aimed to investigate the effect of the long non-coding ribonucleic acid (lncRNA) HOX transcript antisense intergenic RNA (HOTAIR) on apoptosis induced by ischemia-reperfusion injury. Differential lncRNAs in myocardial ischemia rats were screened by a lncRNA microarray and the expression levels of lncRNA HOTAIR and microRNA (miR)-130a-3p were analyzed using reverse transcription-quantitative polymerase chain reaction in hypoxia-induced cardiomyocytes. The mechanism of lncRNA HOTAIR in cardiotoxicity was investigated using cell transfection, lncRNA knockdown, Cell Counting Kit-8, flow cytometry, western blotting, dual luciferase reporter assays and RNA immunoprecipitation. The expression level of lncRNA HOTAIR was significantly downregulated in the ischemic myocardium of rats. Overexpression of HOTAIR in H9c2 (rat cardiomyocyte line) cells could inhibit the apoptosis induced by H2O2. A direct interaction was found between HOTAIR and miR-130a-3p, and mouse double minute 4 (MDM4) was also found to be a potential target of miR-130a-3p. The overexpression of MDM4 in H9c2 cells transfected with miR-130a-3p mimics increased apoptosis, and miR-130a-3p targeted inhibition of MDM4 promoted H2O2-induced apoptosis of H9c2 cells. Overall, HOTAIR was found to inhibit the apoptosis of H9c2 cells induced by H2O2 through the miR-130a-3p/MDM4 axis.