Abstract:

Objective To explore the effect of miR⁃92a⁃3p on glomerular mesangial cell injury induced by high glucose by targeting Homeobox protein 13（HOXA13）and its mechanism. Methods High glucose was used to induce mouse glomerular mesangial cells SV40⁃MES⁃13 to establish a cell injury model. Experimental groups included control group，high glucose group，anti⁃miR⁃NC+ high glucose group，anti⁃miR⁃92a⁃3p+ high glucose group，pcDNA+ high glucose group，pcDNA⁃HOXA13+ high glucose group，anti⁃miR⁃92a⁃3p+ si⁃NC+high glu⁃ cose group，and anti⁃miR⁃92a⁃3p+si⁃HOXA13+high glucose group. QRT⁃PCR and western blot were used to detect the expression of miR⁃92a⁃3p and HOXA13，respectively. Flow cytometry was used to detect the rate of apoptosis； the dual luciferase reporter experiment to detect the targeting relationship between miR⁃92a⁃3p and HOXA13；and western blot to detect the protein expression of Cleaved⁃caspase⁃3，and Cleaved⁃caspase⁃12. Results Compared with those in the control group，the expression of miR⁃92a⁃3p in the high glucose group was increased（P < 0.05）； HOXA13 mRNA and protein levels were decreased（P < 0.05），and the apoptosis rate and the protein levels of Cleaved⁃caspase⁃3，Cleaved⁃caspase⁃12 were increased（P < 0.05）. After transfection of anti⁃miR⁃92a⁃3p or pcDNA⁃ HOXA13，the apoptosis rate and the protein levels of Cleaved⁃caspase⁃3 and Cleaved⁃caspase⁃12 were decreased （P < 0.05）. HOXA13 was a target gene of miR⁃92a⁃3p. Co⁃transfection of anti⁃miR⁃92a⁃3p and si⁃HOXA13 could attenuate the inhibitory effects of anti ⁃miR ⁃ 92a ⁃3p on high glucose induced glomerular mesangial cell apoptosis （P < 0.05）. Conclusion Knocking down miR ⁃ 92a ⁃ 3p can inhibit apoptosis by targeting the expression of HOXA13，thereby reducing the glomerular mesangial cell damage induced by high glucose.

Key words:

glomerular mesangial cells, miR ? 92a ?3p, Homeobox protein 13, apoptosis, high glucose