Microglial peroxiredoxin V acts as an inducible anti-inflammatory antioxidant through cooperation with redox signaling cascades
- Authors
- Sun, Hu-Nan; Kim, Sun-Uk; Huang, Song Mei; Kim, Jin-Man; Park, Young-Ho; Kim, Seok-Ho; Yang, Hee-Young; Chung, Kyoung-Jin; Lee, Tae-Hoon; Choi, Hoon Sung; Min, Ju Sik; Park, Moon-Ki; Kim, Sang-Keun; Lee, Sang-Rae; Chang, Kyu-Tae; Lee, Sang-Ho; Yu, Dae-Yeul; Lee, Dong-Seok
- Issue Date
- 7월-2010
- Publisher
- WILEY
- Keywords
- c-jun N-terminal kinase; lipopolysaccharide; microglia; nitric oxide; peroxiredoxin V; reactive oxygen species
- Citation
- JOURNAL OF NEUROCHEMISTRY, v.114, no.1, pp.39 - 50
- Indexed
- SCIE
SCOPUS
- Journal Title
- JOURNAL OF NEUROCHEMISTRY
- Volume
- 114
- Number
- 1
- Start Page
- 39
- End Page
- 50
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/116155
- DOI
- 10.1111/j.1471-4159.2010.06691.x
- ISSN
- 0022-3042
- Abstract
- P>Reactive oxygen species (ROS) actively participate in microglia-mediated pathogenesis as pro-inflammatory molecules. However, little is known about the involvement of specific antioxidants in maintaining the microglial oxidative balance. We demonstrate that microglial peroxiredoxin (Prx) 5 expression is up-regulated by lipopolysaccharide (LPS) through activation of the ROS-sensitive signaling pathway and is involved in attenuation of both microglial activation and nitric oxide (NO) generation. Unlike in stimulation of oxidative insults with paraquat and hydrogen peroxide, Prx V expression is highly sensitive to LPS-stimulation in microglia. Reduction of ROS level by treatment with either NADPH oxidase inhibitor or antioxidant ablates LPS-mediated Prx V up-regulation in BV-2 microglial cells and is closely associated with the activation of the c-jun N-terminal kinase (JNK) signaling pathway. This suggests the involvement of ROS/JNK signaling in LPS-mediated Prx V induction. Furthermore, NO induces Prx V up-regulation that is ablated by the addition of inducible nitric oxide synthase inhibitor or deleted mutation of inducible nitric oxide synthase in LPS-stimulated microglia. Therefore, these results suggest that Prx V is induced by cooperative action among the ROS, RNS, and JNK signaling cascades. Interestingly, knockdown of Prx V expression causes the acceleration of microglia activation, including augmented ROS generation and JNK-dependent NO production. In summary, we demonstrate that Prx V plays a key role in the microglial activation process through modulation of the balance between ROS/NO generation and the corresponding JNK cascade activation.
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Collections - College of Life Sciences and Biotechnology > Division of Life Sciences > 1. Journal Articles
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