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

Abstract

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. Plasma samples from both patients with MI (n = 65) and healthy controls (n = 65) were subjected to RNA extractions and real-time quantitative polymerase chain reaction 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 real-time quantitative polymerase chain reaction 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. In this study, we found that ACAP2 and mature miR-532 were both upregulated in plasma from patients with MI. ACAP2 and mature miR-532 were inversely correlated, whereas ACAP2 and premature miR-532 were not significantly correlated. In cardiomyocytes, overexpression of ACAP2 increased 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. ACAP2 is overexpressed in MI and may promote the maturation of miR-532 to induce the apoptosis of cardiomyocyte.