Upregulation of circFOXP1 attenuates inflammation and apoptosis induced by ox-LDL in human umbilical vein endothelial cells by regulating the miR-185-5p/BCL-2 axis.

The pathogenesis of coronary artery disease (CAD) is closely related to an abnormal function of the coronary arteries due to myocardial ischemia, hypoxia, or necrosis, which poses a threat to human health. Therefore, this study was conducted to evaluate the role of circFOXP1 in controlling endothelial cell function during atherosclerosis (AS), and further investigate its potential molecular mechanism of regulation. Through Starbase database analysis, we predicted that circFOXP1 can sponge miR-185-5p that targets BCL-2. We found that interleukin (IL)-6, tumor necrois factor (TNF)-α, and IL-1β were significantly upregulated in high-fat diet (HFD)-induced apolipoprotein E-deficient (ApoE/) mice compared with those in the control mice. CircFOXP1 was also significantly upregulated in the AS-mice model and AS-cell model. Moreover, miR-185-5p overexpression was found to inhibit BCL-2 protein expression, which consequently reduced the proliferation, and increased the oxidized low-density lipoprotein (ox-LDL)-induced human umbilical vein endothelial cells (HUVECs) apoptotic rate. Taken together, our data show that circFOXP1 can further aggravate endothelial cell injury by regulating the miR-185-5p/BCL-2 signal axis.