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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. • The expression of miR-320a was decreased in muller cells induced by high glucose; •Overexpression of miR-320a inhibited high glucose-induced angiogenesis in retinal endothelial; •lncRNA MALAT1 inhibited diabetic retinal angiogenesis by sponge miR-320a; •Overexpression of miR-320a inhibited high glucose-induced angiogenesis in retinal endothelial cells by down-regulating HIF-1. [ABSTRACT FROM AUTHOR]