Abstract: Objective To investigate the expression of miR-181a in hydrogen peroxide (H2O2)-injured human umbilical vein endothelial cells (HUVECs) by H2O2, and the effect and mechanism of miR-181a on cell viability and apoptosis. Methods The viability and apoptosis of HUVECs was measured by MTT and flow cytometry assays. miR-181a and X-linked inhibitor of apoptosis (XIAP) expressions were determined by qRT-qCR and Western blot analyses. The binding sites of miR-181a in XIAP 3'UTR were predicted using Targetscan software and verified by Dual-Luciferase and Western blot assays. Results 1) H2O2 inhibited cell activity while promoted apoptosis of HUVECs in a dose-dependent manner (P<0.05). 2) miR-181a was significantly elevated in H2O2-treated HUVECs (P<0.05). 3) Knockdown of miR-181a promoted H2O2-induced cell activity and inhibited apoptosis (P<0.05). 4) XIAP was identified to be a target for miR-181a. 5) Overexpression of miR-181a inhibited H2O2-induced cell activity and promoted apoptosis, which was reversed by XIAP restoration. Conclusions These findings suggested that miR-181a stimulated H2O2-induced cell activity while inhibited cell apoptosis by targeting XIAP, leading to the aggravation of HUVECs injury.

Key words: Hydrogen peroxide, vascular endothelial injury, cell line HUVECs, MiR-181a, X linked inhibitor of apoptosis protein, activity, apoptosis