miR-291b-3p mediated ROS-induced endothelial cell dysfunction by targeting HUR.

Endothelial dysfunction is an early marker of atherosclerosis. Previous studies have indicated that microRNA (miR)‑291b‑3p regulates the metabolism of lipids and glucose in the liver via targeting adenosine monophosphate‑activated kinase α1 and transcription factor p65. The present study investigated whether miR‑291b‑3p mediated H2O2‑mediated endothelial dysfunction. The level of apoptosis of EOMA mouse endothelial cells was analyzed by terminal deoxynucleotidyl‑transferase‑mediated dUTP nick end labelling staining. The mRNA levels of miR‑291b‑3p, intercellular adhesion molecule‑1 (ICAM‑1) and vascular adhesion molecule‑1 (VCAM‑1) were determined by quantitative polymerase chain reaction. The level of phosphorylated extracellular signal‑regulated kinase, and levels of B‑cell lymphoma 2 (Bcl‑2)‑associated X protein and Bcl‑2 protein were detected by western blot analysis. The treatment of H2O2 induced the apoptosis and increased the mRNA levels of miR‑291b‑3p, ICAM‑1 and VCAM‑1 in EOMA cells. It was also demonstrated that the overexpression of miR‑291b‑3p promoted EOMA cell apoptosis and dysfunction. In contrast, the downregulation of miR‑291b‑3p rescued the effect of H2O2 on EOMA cell dysfunction. In addition, Hu antigen R (HuR) was identified as a target gene of miR‑291b‑3p in EOMA cells. The overexpression of HuR reversed the endothelial dysfunction induced by miR‑291b‑3p mimics. The present study provides novel insight into the critical role of miR‑291b‑3p on the endothelial dysfunction induced by H2O2. miR‑291b‑3p may mediate H2O2‑induced endothelial dysfunction via targeting HuR.