LAUSR

Diabetic retinopathy (DR) is a devastating complication of diabetes. The aim of the present study is to investigate the exact role and mechanism of lncRNA MALAT1 (MALAT1) in the progress of DR. Oxygen-induced retinopathy (OIR) mouse model and high glucose (HG)-stimulated human retinal microvascular endothelial cells (HRMECs) were employed to mimic the pathological statues of DR. qRT-PCR or western blot results showed that MALAT1, VEGFA and HIF-1α levels were increased in DR retinal tissues and HG-stimulated HRMECs, whereas the expression of miR-203a-3p was decreased. Knock-down of MALAT1 or up-regulation of miR-203a-3p both suppressed HG-induced proliferation, migration and tube formation of HRMECS. Dual-luciferase reporter assay showed that miR-203a-3p could bind to the predicted seed regions of MALAT1 as evidenced by the reduced luciferase activity. Furthermore, enforced down-regulation of miR-203a-3p abolished the suppressive effect of MALAT1 silencing on HRMECs cell migration and tube formation. In conclusion, these data demonstrated that MALAT1 may affect angiogenesis by sponging miR-203a-3p in DR. MALAT1 may act as a novel therapeutic target for the treatment of DR.