Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5534030 | Molecular and Cellular Endocrinology | 2017 | 11 Pages |
â¢miR-195 was upregulated in the diabetic rat retina and oxidative stressed HMRECs.â¢miR-195 directly targeted the 3â²- UTR of MFN2 mRNA.â¢miR-195 regulated angiogenesis and vascular permeability by inhibiting the expression of MFN2.
This study was performed to investigate the oxidative stress-induced miRNA changes in relation to pathogenesis of diabetic retinopathy (DR) and to establish a functional link between miRNAs and oxidative stress-induced retinal endothelial cell injury. Our results demonstrated that oxidative stress could induce alterations of miRNA expression profile, including up-regulation of miR-195 in the diabetic retina or cultured HMRECs after exposed to H2O2 or HG (PÂ <Â 0.05). Oxidative stress also resulted in a significant reduction of MFN2 expression in diabetic retina or HMRECs (PÂ <Â 0.05). Overexpression of miR-195 reduced MFN2 protein levels, and induced tube formation and increased permeability of diabetic retinal vasculature. The luciferase reporter assay confirmed that miR-195 binds to the 3â² -untranslated region (3â²-UTR) of MFN2 mRNA. This study suggested that miR-195 played a critical role in oxidative stress-induced retinal endothelial cell injury by targeting MFN2 in diabetic rats.