Potential role of 8-oxoguanine DNA glycosylase 1 as a STAT1 coactivator in endotoxin-induced inflammatory response
- Authors
- Kim, Hong Sook; Kim, Byung-Hak; Jung, Joo Eun; Lee, Chang Seok; Lee, Hyun Gyu; Lee, Jung Weon; Lee, Kun Ho; You, Ho Jin; Chung, Myung-Hee; Ye, Sang-Kyu
- Issue Date
- Apr-2016
- Publisher
- ELSEVIER SCIENCE INC
- Keywords
- Coactivator; Endotoxin; Inflammation; OGG1; STAT1
- Citation
- FREE RADICAL BIOLOGY AND MEDICINE, v.93, pp.12 - 22
- Journal Title
- FREE RADICAL BIOLOGY AND MEDICINE
- Volume
- 93
- Start Page
- 12
- End Page
- 22
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/8415
- DOI
- 10.1016/j.freeradbiomed.2015.10.415
- ISSN
- 0891-5849
- Abstract
- Human 8-oxoguanine DNA glycosylase 1 (OGG1) is the major DNA repair enzyme that plays a key role in excision of oxidative damaged DNA bases such as 8-oxoguainine (8-oxoG). Recent studies suggest another function of OGG1, namely that it may be involved in the endotoxin- or oxidative stress-induced inflammatory response. In this study, we investigated the role of OGG1 in the inflammatory response. OGG1 expression is increased in the organs of endotoxin-induced or myelin oligodendrocyte glycoprotein (MOG)-immunized mice and immune cells, resulting in induction of the expression of pro-inflammatory mediators at the transcriptional levels. Biochemical studies showed that signal transducer and activator of transcription 1 (STAT1) plays a key role in endotoxin-induced OGG1 expression and inflammatory response. STAT1 regulates the transcriptional activity of OGG1 through recruiting and binding to the gamma-interferon activation site (GAS) motif of the OGG1 promoter region, and chromatin remodeling by acetylation and dimethylation of lysine-14 and-4 residues of histone H3. In addition, OGG1 acts as a STAT1 coactivator and has transcriptional activity in the presence of endotoxin. The data presented here identifies a novel mechanism, and may provide new therapeutic strategies for the treatment of endotoxin-mediated inflammatory diseases. (C) 2015 Elsevier Inc. All rights reserved.
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