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Knockdown of Tripartite Motif 8 Protects H9C2 Cells Against Hypoxia/Reoxygenation-Induced Injury Through the Activation of PI3K/Akt Signaling Pathway.

Authors
  • Dang, Xiaoyan1
  • Qin, Yong2
  • Gu, Changwei1
  • Sun, Jiangli1
  • Zhang, Rui1
  • Peng, Zhuo1
  • 1 Department of Emergency, 12480The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China. , (China)
  • 2 Department of General Surgery, Xi'an Central Hospital, Xi'an, China. , (China)
Type
Published Article
Journal
Cell Transplantation
Publisher
SAGE Publications
Publication Date
Jan 01, 2020
Volume
29
Identifiers
DOI: 10.1177/0963689720949247
PMID: 32841049
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Tripartite motif 8 (TRIM8) is a member of the TRIM protein family that has been found to be implicated in cardiovascular disease. However, the role of TRIM8 in myocardial ischemia/reperfusion (I/R) has not been investigated. We aimed to explore the effect of TRIM8 on cardiomyocyte H9c2 cells exposed to hypoxia/reoxygenation (H/R). We found that TRIM8 expression was markedly upregulated in H9c2 cells after stimulation with H/R. Gain- and loss-of-function assays proved that TRIM8 knockdown improved cell viability of H/R-stimulated H9c2 cells. In addition, TRIM8 knockdown suppressed reactive oxygen species production and elevated the levels of superoxide dismutase and glutathione peroxidase. Knockdown of TRIM8 suppressed the caspase-3 activity, as well as caused significant increase in bcl-2 expression and decrease in bax expression. Furthermore, TRIM8 overexpression exhibited apposite effects with knockdown of TRIM8. Finally, knockdown of TRIM8 enhanced the activation of PI3K/Akt signaling pathway in H/R-stimulated H9c2 cells. Inhibition of PI3K/Akt by LY294002 reversed the effects of TRIM8 knockdown on cell viability, oxidative stress, and apoptosis of H9c2 cells. These present findings defined TRIM8 as a therapeutic target for attenuating and preventing myocardial I/R injury.

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