LncRNA Meg3 promotes oxygen and glucose deprivation injury by decreasing angiogenesis in hBMECs by targeting the miR‑122‑5p/NDRG3 axis

• Published in: Experimental and therapeutic medicine Vol. 24; no. 4
• Main Authors: Luo, Zhaoliang, Gong, Tingliang, Li, Weihong, Tao, Wenqiang
• Format: Journal Article
• Language: English
• Published: Athens Spandidos Publications 01.10.2022; Spandidos Publications UK Ltd; D.A. Spandidos
• Subjects: Angiogenesis; Apoptosis; Binding sites; Brain; Genetic aspects; Glucose; Glucose metabolism; Health aspects; Laboratories; MicroRNA; MicroRNAs; Neovascularization; Oxygen consumption; Proteins; Software; Statistical analysis; Wound healing; China
• ISSN: 1792-0981; 1792-1015
• DOI: 10.3892/etm.2022.11559

Oxygen-glucose deprivation (OGD) is widely used as an in vitro model for stroke. The present study aimed to explore the mechanisms of action of long non-coding RNA (lncRNA) maternally expressed gene 3 (Meg3) in angiogenesis following OGD. The human brain microvascular endothelial cell line, hCMEC/D3, was used to establish the OGD model. lncRNA Meg3 was highly expressed in hCMEC/D3 cells subjected to OGD. Furthermore, it was found that the overexpression of lncRNA Meg3 decreased the proliferation, migration and angiogenesis of hCMEC/D3 cells subjected to OGD, and increased cell apoptosis. Meg3 silencing exerted the opposite effects. Subsequently, lncRNA Meg3 increased the expression of NDRG family member 3 (NDRG3) by directly binding to miR-122-5p. The overexpression of miR-122-5p and the knockdown of NDRG3 reversed the inhibitory effects of Meg3 overexpression on the proliferation, migration and angiogenesis of hCMEC/D3 cells subjected to OGD, as well as the promoting effects of Meg3 overexpression on cell apoptosis. The present study demonstrated that lncRNA Meg3 functions as a competing endogenous RNA by targeting the miR-122-5p/NDRG3 axis in regulating OGD injury.