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LNCRNA Gas5 suppression protected Hl-1 cells against hypoxia injury by sponging Mir-222-3p.

Authors
  • He, Jie1
  • Dai, Henhua1
  • Zhao, Qian1
  • Guo, Jianshu2
  • Chen, Chi3
  • 1 Department of Cardiology, Chong Gang General Hospital, Chong Qing, China. , (China)
  • 2 Department of gerontology, Hospital of the University of Electronic Science and Technology of China and Sichuan Provincial people's Hospital, Chengdu, Sichuan Province 610072, China. , (China)
  • 3 Department of gerontology, Hospital of the University of Electronic Science and Technology of China and Sichuan Provincial people's Hospital, Chengdu, Sichuan Province 610072, China. Electronic address: [email protected] , (China)
Type
Published Article
Journal
Experimental and Molecular Pathology
Publisher
Elsevier
Publication Date
Aug 01, 2020
Volume
115
Pages
104436–104436
Identifiers
DOI: 10.1016/j.yexmp.2020.104436
PMID: 32240616
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Hypoxia may cause diseases in human beings. The up- or down- regulation of lncRNAs were identified to possess the ability to protect the myocardial cells from hypoxia injury. This study explored the role of lncRNA GAS5 in sodium Hydrosulfite Induced Hl-1 Cells in vitro. RT-qPCR was applied to measure the expressions of RNAs whereas the cell viability was detected with CCK-8. Luciferase report assay was performed to validate the binding between lncRNA GAS5 and miR-222-3p. The proteins regarding PI3K/AKT signaling were evaluated through western blot analysis. The results showed that the hypoxia could reduce cell viabilities and enhance the apoptosis. Meanwhile, the PI3K/AKT signaling pathway was suppressed as well. lncRNA GAS5 got expressed higher in hypoxic cells whereas the suppressed GAS5 was able to increase cell viabilities while inhibiting apoptosis. MiR-222-3p was the target gene of lncRNA as determined by the luciferase report assay and its expressions were low in hypoxic cells. The overexpressed miR-222-3p could promote proliferation and inhibit apoptosis. Then, the correlation of GAS5 and miR-222-3p was measured which showed that miR-222-3p could resume the functions of GAS5 in cell viabilities and apoptosis through protein regulation in PI3K and AKT signaling pathways. Copyright © 2020. Published by Elsevier Inc.

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