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Long non-coding RNA NEAT1 inhibits oxidative stress-induced vascular endothelial cell injury by activating the miR-181d-5p/CDKN3 axis.

Authors
  • Zhang, Min1
  • Wang, Xueting1
  • Yao, Jing2
  • Qiu, Zhaohui1
  • 1 a Division of Cardiology, TongRen Hospital, Shanghai Jiao Tong University School of Medicine , Shanghai , China. , (China)
  • 2 b Division of Cardiology, Huadong Hospital affiliated with Fudan University , Shanghai , China. , (China)
Type
Published Article
Journal
Artificial Cells Nanomedicine and Biotechnology
Publisher
Informa UK (Taylor & Francis)
Publication Date
Dec 01, 2019
Volume
47
Issue
1
Pages
3129–3137
Identifiers
DOI: 10.1080/21691401.2019.1646264
PMID: 31352814
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Endothelial cell (EC) dysfunction induces atherosclerotic coronary heart disease (CHD) development. Recent studies demonstrated that lncRNA NEAT1 mediates multiple biological functions of cells. How NEAT1 regulates EC function is still unclear, so this study explored the role and mechanism of NEAT1 in oxidative stress-induced ECs. The levels of NEAT1 and miR-181d-5p were measured in serum samples from ApoE-/- mice and t-BHP-treated human umbilical vein endothelial cells (HUVECs) by qRT-PCR. The potential role of NEAT1 in viability, migration and apoptosis was analyzed by CCK-8, cell metastasis, flow cytometry, dual-luciferase reporter, RNA immunoprecipitation and Western blot assays using HUVECs overexpressing NEAT1. The expression of NEAT1 was increased, but miR-181d-5p expression was decreased in serum samples from both ApoE-/- mice and t-BHP-treated HUVECs. Overexpression of NEAT1 increased viability, migration and CDKN3 expression but decreased apoptotic rates, caspase-3 activity and miR-181d-5p expression in HUVECs. In addition, NEAT1 acted as a promoter of the proangiogenic capacity of HUVECs by targeting miR-181d-5p/CDKN3. Altogether, these findings indicate that NEAT1 may exert a protective effect on HUVECs by regulating the miR-181d-5p/CDKN3A axis.

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