AIM: To study the effect of miR-221 on apoptosis of high glucose-induced human retinal vascular endothelial cells and to explore its mechanism.

METHODS: High-glucose-induced HRCECs were established by treatment of HRCECs cells with glucose at 30mmol/L for 48h; HG+miR-NC group(transfected miR-NC), HG+miR-221 group(transfected miR-221 mimics), HG+anti-miR-NC group(transfected anti-miR-NC), HG+anti-miR-221 group(transfected anti-miR-221), HG+miR-221+pcDNA 3.1 group(co-transfected miR-221 mimics and pcDNA 3.1), HG+miR-221+pcDNA 3.1-MDM2 group(co-transfected miR-221 mimics and pcDNA 3.1-MDM2), transfected into HRCECs cells by liposome method, and then treated with high glucose; qRT-PCR method for detection the expression of miR-221, p53 and MDM2; the protein expression of p53 and MDM2 were detected by Western blot. The apoptosis of cells was detected by flow cytometry.

RESULTS: Compared with NG group, the expression of miR-221 and p53 was significantly increased, the expression of MDM2 was significantly decreased, and the apoptosis rate was significantly increased in high glucose-induced HRCECs. Overexpression of miR-221 induced apoptosis of high glucose-induced HRCECs cells is more obvious. Inhibition of miR-221 can down-regulate the apoptosis of high glucose-induced HRCECs and down-regulate p53, up-regulate MDM2; overexpression of MDM2 can reverse the inhibition by miR-221 anti-apoptotic effect of cells and regulation of p53 and MDM2 of high-glucose-induced HRCECs.

CONCLUSION: miR-221 can promote the apoptosis of high-glucose-induced human retinal vascular endothelial cells, and its mechanism is related to p53/MDM2 signaling pathway.