LncRNA MALAT1 aggravates the retinal angiogenesis via miR-320a/HIF-1α axis in diabetic retinopathy.

Diabetic retinopathy (DR) is one of the most serious microvascular complications of diabetes and an important cause of blindness in adults. In previous study, we found that miR-320a alleviated the damage of muller cells in DR. In this study, we mainly explored the mechanism of lncRNA MALAT1 on retinal angiogenesis in DR by regulating miR-320a/HIF-1α. The expression of MALAT1 and miR-320a was detected by RT-qPCR, and the expression of HIF-1α was detected by Western blot. The superoxide anion level, invasion, angiogenesis, and vascular permeability of mouse retinal microvascular endothelial cells (MRMECs) co-cultured with muller cells were evaluated by dihydroethidium, transwell, angiogenesis and immunofluorescence assay. In order to analyze the targeting relationship between miR-320a and MALAT1 or HIF-1α, we performed dual luciferase reporter gene, fluorescence in situ hybridization (FISH), RNA immunoprecipitation (RIP) and RNA pulldown experiments. The results should that MALAT1 and HIF-1α were highly expressed and miR-320a was low expressed in high glucose (HG)-induced muller cells, and MALAT1 could competitively bind with HIF-1α. Knocking down miR-320a inhibited MRMECs invasion angiogenesis, and vascular permeability by targeting miR-320a. Overexpression of miR-320a down regulated HIF-1α and inhibited the invasion, angiogenesis, and vascular permeability of MRMECs. In conclusion, MALAT1 inhibits HIF-1α expression and MRMECs angiogenesis in DR through spongy miR-320a.