The upregulation of miR-101 promotes vascular endothelial cell apoptosis and suppresses cell migration in acute coronary syndrome by targeting CDH5.

MicroRNAs (miRNAs) have been reported to be of great importance in a wide range of physiological and pathological processes, including acute coronary syndrome (ACS). However, the exact role of miRNAs in the pathogenesis of ACS has not been fully elucidated. In this study, we found that miR-101 was significantly upregulated in the serum samples of patients with acute coronary syndrome compared with healthy controls. In human umbilical vein endothelial cells (HUVECs), the overexpression of miR-101 drastically promoted cell apoptosis and inhibited cell migration. Mechanistically, miR-101 repressed the expression of CHD5 by targeting its 3'-untranslated region (3'UTR). The silencing of CHD5 also induced cell apoptosis and suppressed cell migration in HUVECs. Taken together, our findings suggest that the miR-101-CHD5 axis may play an important role in the biological behaviors of endothelial cells during the pathogenesis of ACS and may afford an effective diagnostic marker and a powerful therapy for this disease. IJCEP