Abstract
Aims: Myocardial infarction (MI) is a type of cardiovascular disease caused by myocardial necrosis. Growing evidences have suggested that circular RNAs (circRNAs) play crucial roles in cardiac hypoxia/reoxygenation (H/R)-induced injury of MI. Methods and results: Hypoxia/reoxygenation model of H9C2 cells was established and circ_0001206 expression was detected via quantitative real-time polymerase chain reaction. Ribonuclease R (RNase R) and Actinomycin D (Act D) assays verified the stability. Cell counting kit-8 (CCK-8), western blot, TUNEL, and flow cytometry assays evaluated cell viability and cell apoptosis. RNA pull-down, RNA binding protein immunoprecipitation (RIP), and luciferase reporter assays explored the mechanisms underlying MI. All experimental data were presented with mean ± standard deviation (SD) and P < 0.05 indicated statistical significance. Circ_0001206 was low-expressed in H9C2 cells under H/R treatment. Circ_0001206 was formed by cyclization of CRK like proto-oncogene, adaptor protein (CRKL). Circ_0001206 overexpression promoted cell viability and inhibited cardiomyocyte apoptosis. It was confirmed that circ_0001206 regulated CRKL expression via acting as a competing endogenous RNA (ceRNA) of microRNA-665 (miR-665). CRKL played a protective role in MI. Conclusions: Circ_0001206 regulates miR-665/CRKL axis to alleviate H/R-induced cardiomyocyte injury in MI. Our findings suggest that circ_0001206 might be a potential target for MI treatment.