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

J. Yang, F.-J. Yang, Y.-G. Wang, G.-F. Su, X. Miao

Department of Ophthalmology, The Second Hospital of Jilin University, Changchun, China. sugf2012@163.com

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• Ophthalmology

OBJECTIVE: The aim of this study was to elucidate the potential influence of MIR497HG on regulating proliferative capacity of human retinal endothelial cells (HRECs).

MATERIALS AND METHODS: 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.

RESULTS: 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.

CONCLUSIONS: 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.

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