MicroRNA-423-5p mediates H2O2-induced apoptosis in cardiomyocytes through O-GlcNAc transferase

Abstract

Reactive oxygen species (ROS) have been clinically shown to be relevant in the progression of various apoptosis-associated heart diseases. Our previous study demonstrated that microRNA (miR)-423-5p is involved in congestive heart failure (CHF) through the direct targeting of O-GlcNAc transferase and the induction of apoptosis in cardiomyocytes. However, the role of miR-423-5p during ROS-induced apoptosis remains to be elucidated. In the present study, the expression of miR-423-5p in cardiomyocytes following exposure to H2O2 was determined using reverse transcription-quantitative polymerase chain reaction analysis. In addition, the effects of silencing of miR-423-5p, by using an miR-423-5p-mimic during H2O2 treatment, on cardiomyocyte apoptosis were detected using a terminal deoxynucleotidyl transferase-deoxyuridine triphosphate nick-end labeling assay. The expression levels of the direct target of miR-423-5p and associated downstream targets were also examined. The results demonstrated that H2O2 significantly induced the expression of miR-423-5p in cardiomyocytes, in a time- and concentration-dependent manner. The silencing of miR-423-5p by transfection with the miR-423-5p-mimic eliminated the H2O2-induced cardiomyocyte apoptosis and decrease in viability. The expression levels of the downstream targets of miR423-5p were also increased by H2O2, and were decreased following the silencing of miR-423-5p. Collectively, the results of the present study demonstrated that miR-423-5p mediated H2O2-induced apoptosis in the cardiomyocytes. Silencing of miR-423-5p significantly protected the cardiomyocytes from H2O2-induced apoptosis, and this may provide a novel therapeutic target for apoptosis-associated heart diseases.