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β-8-Oxoguanine DNA Glycosylase Overexpression Reduces Oxidative Stress-Induced Mitochondrial Dysfunction and Apoptosis Through the JNK Signaling Pathway in Human Bronchial Epithelial Cells.

Authors
  • Lin, Ziying1
  • Xu, Wenya1, 2
  • Li, Chunyan1, 2
  • Wang, Yahong1
  • Yang, Lawei1
  • Zou, Bao'an1, 2
  • Gao, Shenglan1
  • Yao, Weimin2
  • Song, Zeqing2
  • Liu, Gang1, 2
  • 1 1 Clinical Research Center, Affiliated Hospital of Guangdong Medical University , Zhanjiang, China . , (China)
  • 2 2 Department of Respiratory Medicine, Affiliated Hospital of Guangdong Medical University , Zhanjiang, China . , (China)
Type
Published Article
Journal
DNA and Cell Biology
Publisher
Mary Ann Liebert
Publication Date
Dec 01, 2017
Volume
36
Issue
12
Pages
1071–1080
Identifiers
DOI: 10.1089/dna.2017.3769
PMID: 29227732
Source
Medline
Keywords
License
Unknown

Abstract

8-Oxoguanine DNA glycosylase (OGG1) is responsible for repairing 8-oxo-7,8-dihydroguanine (8-oxoG). Our previous study demonstrated that α-OGG1 protects cells from oxidative damage-induced apoptosis and mitochondrial dysfunction in human lung cancer cells. However, the function of β-OGG1 remains to be elucidated. In this study, we demonstrated that overexpressed β-OGG1 has the same role as α-OGG1 in protecting human bronchial epithelial cells from apoptosis and mitochondrial dysfunction. Furthermore, flow cytometry, confocal microscopy, and western blotting showed that the overexpression of β-OGG1 could block oxidant-induced apoptosis in human bronchial epithelial cells. Additionally, knocking down OGG1 enhanced oxidative damage-induced apoptosis and mitochondrial dysfunction, whereas the overexpression of β-OGG1 had the opposite effects and led to the downregulation of Bax and PARP. The antiapoptotic function of β-OGG1 involved the JNK signaling pathway. These findings suggest that β-OGG1 and α-OGG1 have a similar function on preventing oxidative damage-mediated apoptosis and mitochondrial dysfunction; these effects might be important in the molecular events underlying oxidant-induced cytotoxicity.

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