Downregulation of microRNA-106a-5p alleviates ox-LDL-mediated endothelial cell injury by targeting STAT3

The apoptosis of endothelial cells (ECs) induced by oxidized low-density lipoprotein (ox-LDL) is an important contributing factor in the pathogenesis of atherosclerosis. It has been reported that microRNA (miR)-106a-5p is overexpressed in atherosclerotic plaques and involved in angiogenesis. However, its role and underlying mechanisms in ox-LDL induced EC apoptosis remain to be fully understood. In the present study the expression of miR-106a-5p in human umbilical vein ECs (HUVECs) stimulated with ox-LDL was investigated using reverse transcription-quantitative PCR analysis. Cell viability and apoptosis were assessed by MTT assay and flow cytometry, respectively. Caspase-3 activity and reactive oxygen species (ROS) levels were determined by commercial kits. The interaction between miR-106a-5p and signal transducer and activator of transcription 3 (STAT3) mRNA was examined by luciferase reporter assay. It was found that ox-LDL treatment significantly increased the levels of miR-106a-5p in a dose-dependent manner in HUVECs. Moreover, these results demonstrated that ox-LDL treatment inhibited cell viability, promoted cell apoptosis, increased caspase-3 activity and ROS levels, whereas inhibition of miR-106a-5p reversed the effects of ox-LDL on HUVECs. In addition, it was shown that STAT3 is a direct target of miR-106a-5p in HUVECs, and silencing of STAT3 impaired the protective effects of miR-106a-5p inhibition on cell apoptosis and oxidative injury induced by ox-LDL. Collectively, these results indicated that miR-106a-5p participated in ox-LDL-stimulated apoptosis and oxidative injury in HUVECs by regulating STAT3. Thus, suggesting that miR-106a-5p/STAT3 may serve as a novel therapeutic target for atherosclerosis in the future.