Overexpression of microRNA-130a-3p suppresses glucose lipid levels and oxidative damage in diabetic retinopathy mice via modulating cell division cycle 42.

Abstract

MicroRNA (miR)-130a-3p has been unraveled to exert effects on diabetes. However, the research for probing its role in diabetic retinopathy (DR) is limited. Our study intends to unravel the regulatory effects of miR-130a-3p on DR development via cell division cycle 42 (CDC42). The DR mouse model was established and the serum sample of DR patients was collected. The levels of miR- 130a-3p and CDC42 in DR mice and patients were detected. The nucleic acids modified miR-130a-3p or CDC42 were injected into DR mice to examine the change of glucose lipid levels, visual acuity, oxidative response and the distribution and expression of CDC42 in retinal tissues in DR mice. The target relationship between miR-130a-3p and CDC42 was confirmed. MiR-130a-3p expression was reduced while CDC42 levels were elevated in DR (P<0.05). The upregulation of miR-130a-3p could hinder glucose lipid levels, improve the visual acuity, relieve the oxidative response and decrease CDC42 expression levels in DR mice (P<0.05). The CDC42 elevation reversed the positive effects of upregulated miR-130a-3p on DR progression (P<0.05). MiR-130a-3p targeted CDC42. The elevated miR-130a-3p relieves glucose lipid levels and oxidative damage in DR by modulating CDC42. The study provides novel therapeutic targets for DR treatment.