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
- 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.