CircRNA ACAP2 is Overexpressed in Myocardial Infarction and Promotes the Maturation of miR-532 to Induce the Apoptosis of Cardiomyocyte

Abstract Background: CircRNA ACAP2 and miR-532 both promotes the apoptosis of cardiomyocytes, which contributes to myocardial infarction (MI). Therefore, ACAP2 and miR-532 may interact with each other to participate in MI. Method: Plasma samples from both MI patients (n=65) and healthy controls (n=65) were subjected to RNA extractions and RT-qPCR to analyze the expression of ACAP2, mature miR-532 and premature miR-532. Correlations among them were analyzed by Pearson’s correlation coefficient. Expression of both mature miR-532 and premature miR-532 in cardiomyocytes with ACAP2 overexpression was analyzed by RT-qPCR to study the effects of ACAP2 overexpression on the maturation of miR-532. The role of ACAP2 and miR-532 in regulating the apoptosis of cardiomyocytes induced by hypoxia was analyzed by cell apoptosis assay. Results: In this study we found that ACAP2 and mature miR-532 were both upregulated in plasma from MI patients. ACAP2 and mature miR-532 were inversely correlated, while ACAP2 and premature miR-532 were not closely correlated. In cardiomyocytes, overexpression of ACAP2 decreased the expression of mature miR-532, but not premature miR-532. Cell apoptosis analysis showed that ACAP2 and miR-532 overexpression promoted the apoptosis of cardiomyocytes induced by hypoxia treatment. In addition, miR-532 inhibitor reduced the effects of ACAP2 overexpression. Conclusion: Therefore, ACAP2 is overexpressed in MI and may promote the maturation of miR-532 to induce the apoptosis of cardiomyocyte.