Abstract
Ischemic heart disease (IHD) is a prominent global cause of morbidity and death resulting from the narrowing or blockage of cardiac coronary arteries. Exposing isolated cardiac myocytes to hypoxia-reoxygenation (H/R) might be an efficient tool to investigate the etiology and underlying mechanism of myocardial ischemia-reperfusion (I/R) injury. This study found that miR-7015 is upregulated in mouse myocardial tissues after I/R injury and in cardiomyocytes after H/R injury. A model of H/R-induced cardiomyocyte injury was established; miR-7015 overexpression exacerbated while miR-7015 inhibition partially ameliorated H/R-induced cardiomyocyte injury by inhibiting cytokine release, promoting cell viability, and suppressing apoptosis. Bioinformatics and experimental studies have identified nuclear factor-kappa-B-inhibitor alpha (Nfkbia) as a direct downstream target of miR-7015. miR-7015 inhibited Nfkbia expression. Unlike miR-7015 overexpression, Nfkbia overexpression alleviated H/R-induced injury in cardiomyocytes. Moreover, Nfkbia overexpression partially abolished the effects of miR-7015 overexpression on H/R-induced cardiomyocyte injury. In conclusion, the miR-7015/Nfkbia axis modulates cardiomyocyte injury induced by H/R, possibly through the NF-κB signaling.