LncRNA MIR497HG inhibits proliferation and migration of retinal endothelial cells under high-level glucose treatment via miRNA-128-3p/SIRT1 axis.

Abstract

The aim of this study was to elucidate the potential influence of MIR497HG on regulating proliferative capacity of human retinal endothelial cells (HRECs). Relative expression levels of MIR497HG, microRNA-128-3p (miRNA-128-3p) and SIRT1 in HRECs treated with different doses of glucose and mannitol were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Dual-Luciferase reporter gene assay was conducted to assess the interaction among MIR497HG, miRNA-128-3p, and SIRT1. In addition, the potential effects of MIR497HG/miRNA-128-3p/SIRT1 axis on proliferative and migratory capacities in HRECs were evaluated by Cell Counting Kit-8 (CCK-8), 5-Ethynyl-2'- deoxyuridine (EdU) and transwell assay, respectively. High-level glucose (HG) treatment significantly downregulated MIR497HG and SIRT1 expression, whereas upregulated miRNA-128-3p expression in HRECs (p<0.05). MiRNA-128-3p was the target gene binding MIR497HG, and SIRT1 was the downstream gene of miRNA-128-3p. Overexpression of MIR497HG significantly attenuated proliferative and migratory abilities of HG-induced HRECs (p<0.05). Furthermore, decreased trends were partially reversed by overexpression of miRNA-128-3p or knockdown of SIRT1. MIR497HG is downregulated after HG treatment. In addition, it suppresses the proliferation and migration of HRECs by targeting miRNA-128-3p/SIRT1 axis, thus influencing the progression of diabetic retinopathy.