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.
In conclusion, CGA inhibits retinal neoangiogenesis during the process of DR by abrogating HG-induced HIF-1α-mediated paracrine VEGF expression in microglia cells and inhibiting VEGF-induced angiogenesis in retinal endothelial cells.
Here, we have demonstrated that its intraocular administration in a rat model of diabetic retinopathy has reduced expression of HIF-1α, HIF-2α, and VEGF by increasing HIF-3α levels.