LncRNA Meg3 promotes oxygen and glucose deprivation injury by decreasing angiogenesis in hBMECs by targeting the miR‑122‑5p/NDRG3 axis
- Zhaoliang Luo
- Tingliang Gong
- Weihong Li
- Wenqiang Tao
Affiliations: Research and Innovation Center, Basic Medical College, Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan 611137, P.R. China, Department of Brain Diseases, Chongqing Traditional Chinese Medicine Hospital, Chongqing 400000, P.R. China
- Published online on: August 11, 2022 https://doi.org/10.3892/etm.2022.11559
Copyright: © Luo
et al. This is an open access article distributed under the
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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.