miR-365 promotes diabetic retinopathy through inhibiting Timp3 and increasing oxidative stress. 
miRs play critical roles in oxidative stress-related retinopathy pathogenesis.  miR-365 was identified in a previously constructed library from glyoxal-treated rat Müller cell.  This report explores epigenetic alterations in Müller cells under oxidative stress to develop a novel therapeutic strategy.  To examine the miR-365 expression pattern, in situ hybridization and quantitative RT-PCR were performed.  Bioinformatical analysis and dual luciferase report assay were applied to identify and confirm target genes.  Streptozotocin (STZ)-treated rats were used as the diabetic retinopathy (DR) model.  Lentivirus-mediated anti-miR-365 was delivered subretinally and intravitreally into the rats' eyes.  The functional and structural changes were evaluated by electroretinogram (ERG), histologically, and through examination of expression levels of metallopeptidase inhibitor 3 (Timp3), glial fibrillary acidic protein (Gfap), recoverin (Rcvrn) and vascular endothelia growth factor A (Vegfa).  Oxidative stress factors and pro-inflammatory cytokines were analyzed.  miR-365 expression was confirmed in the glyoxal-treated rat Müller cell line (glyoxal-treated rMC-1).  In the retina, miR-365 mainly localized in the inner nuclear layer (INL).  The increased miR-365 participated in Müller cell gliosis through oxidative stress aggravation, as observed in glyoxal-treated rMC-1 and DR rats before 6 weeks.  Timp3 was a target and negatively regulated by miR-365.  When miR-365 was inhibited, Timp3 expression was upregulated, Müller cell gliosis was alleviated, and retinal oxidative stress was attenuated.  Visual function was also partially rescued as detected by ERG.  miR-365 was found to be highly expressed in the retina and the abnormality of miR-365/Timp3 pathway is closely related to the pathology, like Müller gliosis, and the visual injury in DR.  The mechanism might be through oxidative stress, and miR-365/Timp3 could be a potential therapeutic target for treating DR.