Abstract:Aim To investigate the effect of miR-152-3p targeting thioredoxin-interacting protein (TXNIP) on the apoptosis of endothelial progenitor cells (EPC) induced by hydrogen peroxide (H2O2). Methods Endothelial progenitor cells were isolated from the peripheral blood of healthy people and identified, a H2O2-induced endothelial progenitor cells damage model (500 μmol/L H2O2 treated for 8 h) was established and the expression of miR-152-3p in endothelial progenitor cells was detected by RT-qPCR. After overexpression of miR-152-3p or inhibition of TXNIP expression or overexpression of miR-152-3p and TXNIP simultaneously in endothelial progenitor cells, they were treated with 500 μmol/L H2O2 for 8 h, the expression level of miR-152-3p, cell apoptosis rate and TXNIP, Bax, Bcl-2, and Caspase-3 protein expression levels were measured; dual luciferase reporter gene experiment was performed to verify the relationship between miR-152-3p and TXNIP. Results Endothelial progenitor cells were successfully isolated from the peripheral blood of healthy people, and the expression level of miR-152-3p in H2O2-induced endothelial progenitor cells decreased by 65.0% (P＜0.001). Compared with the control group, the apoptosis rate, Bax and Caspase-3 protein expression levels in the model group increased by 895.1%, 352.0% and 290.3%, and the Bcl-2 expression level decreased by 79.4% (all P＜0.001). Compared with the miR-NC group, the apoptosis rate and the protein expression levels of Bax and Caspase-3 in the miR-152-3p mimic group decreased by 55.7%, 60.9% and 56.8% (P＜0.001), and the protein expression level of Bcl-2 increased by 389.5% (all P＜0.001). Compared with the si-NC group, the apoptosis rate and the protein expression levels of TXNIP, Bax and Caspase-3 in the si-TXNIP group were decreased by about 40.2%, 57.5%, 59.8% and 55.4% (all P＜0.001). Compared with miR-152-3p mimic＋pcDNA group, the apoptosis rate, TXNIP, the protein expression levels of Bax and Caspase-3 increased by 86.8%, 184.8%, 137.7% and 109.2% (P＜0.001), and the protein expression level of Bcl-2 decreased by 69.1% (P＜0.001). The results of dual luciferase reporter gene experiments showed that miR-152-3p was able to target and negatively regulate TXNIP expression. Conclusion MiR-152-3p was under-expressed in H2O2-induced endothelial progenitor cells. Overexpression of miR-152-3p can inhibit H2O2-induced endothelial progenitor cell apoptosis by targeting the expression of TXNIP.
