Abstract
Circular RNA (circRNA) MFACR promotes cardiomyocyte death that leads to myocardial infarction (MI). This study aimed to explore the role of MFACR in MI. T-qPCRs were performed to measure the expression levels of MFACR and miR-125b in plasma samples from both MI patients (n = 61) and healthy controls (n = 61). MFACR or miR-125b was overexpressed in AC16 cells (cardiomyocytes) to explore the interaction between them. Methylation of miR-125b gene in cells with the overexpression of MFACR was detected by methylation-specific PCR. Cell apoptosis after transfections was detected by cell apoptosis assay. MI model was constructed to further demonstrate the effect of MFACR in vivo. We found that MFACR was upregulated in MI and inversely correlated with miR-125b. In AC16 cells, hypoxia treatment increased the expression levels of MFACR and decreased the expression levels of miR-125b. In AC16 cells, overexpression of MFACR decreased the expression levels of miR-125b and increased the methylation of miR-125b gene. Under hypoxia treatment, overexpression of MFACR increased AC16 cell apoptosis, and overexpression of miR-125b decreased cell apoptosis. In addition, overexpression of miR-125b reversed the effects of overexpression of MFACR on cell apoptosis both in vivo and in vitro.