Circ_0001206 regulates miR‐665/CRKL axis to alleviate hypoxia/reoxygenation‐induced cardiomyocyte injury in myocardial infarction

Abstract

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.

Keywords

• circ_0001206
• miR‐665
• CRKL
• Myocardial infarction