LAUSR

Atherosclerosis (AS) is a chronic inflammatory disease characterized by the formation of atherosclerotic plaque in the intima of arteries. Among the known regulators of atherosclerosis, microRNAs (miRNAs) have been reported to play critical roles in lipoprotein homeostasis and plaque formation. But the roles of microRNA‐125a‐3p (miR‐125a‐3p) in the pathogenesis of AS remain unknown. Human umbilical vein endothelial cells (HUVECs) were treated with oxidized low‐density lipoprotein (ox‐LDL) to construct the vascular injury model of AS pathogenesis in vitro. miR‐125a‐3p and BMP and activin membrane‐bound inhibitor (BAMBI) expression levels in HUVECs were then measured by quantitative real‐time polymerase chain reaction and western blot. The viability and apoptosis of HUVECs were analyzed by Cell Counting Kit‐8 assay, TUNEL assay, and flow cytometry, respectively. The relationship between BAMBI 3′‐untranslated region and miR‐125a‐3p was validated by dual luciferase reporter gene assay. miR‐125a‐3p expression was raised in HUVECs induced with ox‐LDL. In HUVECs, miR‐125a‐3p enhanced the effects of ox‐LDL treatment on repressing the viability and promoting the apoptosis of cells. Additionally, BAMBI was confirmed as a direct target of miR‐125a‐3p and BAMBI overexpression reversed the effects of miR‐125a‐3p on HUVECs. miR‐125a‐3p aggravates the dysfunction of HUVECs induced by ox‐LDL via BAMBI, which implies that miR‐125a‐3p is involved in the pathogenesis of AS.