Microglial peroxiredoxin V acts as an inducible anti-inflammatory antioxidant through cooperation with redox signaling cascades

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dc.contributor.authorH N Sun-
dc.contributor.authorSun-Uk Kim-
dc.contributor.authorS M Huang-
dc.contributor.authorJ M Kim-
dc.contributor.authorYoung-Ho Park-
dc.contributor.authorSeok Ho Kim-
dc.contributor.authorH Y Yang-
dc.contributor.authorK J Chung-
dc.contributor.authorT H Lee-
dc.contributor.authorH S Choi-
dc.contributor.authorJ S Min-
dc.contributor.authorM K Park-
dc.contributor.authorS K Kim-
dc.contributor.authorSang Rae Lee-
dc.contributor.authorKyu Tae Chang-
dc.contributor.authorS H Lee-
dc.contributor.authorDae Yeul Yu-
dc.contributor.authorD S Lee-
dc.date.accessioned2017-04-19T09:18:45Z-
dc.date.available2017-04-19T09:18:45Z-
dc.date.issued2010-
dc.identifier.issn00223042-
dc.identifier.uri10.1111/j.1471-4159.2010.06691.xko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/9550-
dc.description.abstractReactive 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.-
dc.publisherWiley-
dc.titleMicroglial peroxiredoxin V acts as an inducible anti-inflammatory antioxidant through cooperation with redox signaling cascades-
dc.title.alternativeMicroglial peroxiredoxin V acts as an inducible anti-inflammatory antioxidant through cooperation with redox signaling cascades-
dc.typeArticle-
dc.citation.titleJournal of Neurochemistry-
dc.citation.number1-
dc.citation.endPage50-
dc.citation.startPage39-
dc.citation.volume114-
dc.contributor.affiliatedAuthorSun-Uk Kim-
dc.contributor.affiliatedAuthorYoung-Ho Park-
dc.contributor.affiliatedAuthorSang Rae Lee-
dc.contributor.alternativeNameSun-
dc.contributor.alternativeName김선욱-
dc.contributor.alternativeNameHuang-
dc.contributor.alternativeName김진만-
dc.contributor.alternativeName박영호-
dc.contributor.alternativeName김석호-
dc.contributor.alternativeName양희영-
dc.contributor.alternativeName정경진-
dc.contributor.alternativeName이태훈-
dc.contributor.alternativeName최훈성-
dc.contributor.alternativeName민주식-
dc.contributor.alternativeName박문기-
dc.contributor.alternativeName김상근-
dc.contributor.alternativeName이상래-
dc.contributor.alternativeName장규태-
dc.contributor.alternativeName이상호-
dc.contributor.alternativeName유대열-
dc.contributor.alternativeName이동석-
dc.identifier.bibliographicCitationJournal of Neurochemistry, vol. 114, no. 1, pp. 39-50-
dc.identifier.doi10.1111/j.1471-4159.2010.06691.x-
dc.subject.keywordC-jun N-terminal kinase-
dc.subject.keywordLipopolysaccharide-
dc.subject.keywordMicroglia-
dc.subject.keywordNitric oxide-
dc.subject.keywordPeroxiredoxin V-
dc.subject.keywordReactive oxygen species-
dc.subject.localC-jun N-terminal kinase-
dc.subject.localc-Jun N-terminal kinase-
dc.subject.localLipopolysaccharide-
dc.subject.localMicroglia-
dc.subject.localNitric oxide-
dc.subject.localNitric oxide (NO)-
dc.subject.localPeroxiredoxin V-
dc.subject.localReactive oxygen species-
dc.subject.localReactive oxygen species (ROS)-
dc.description.journalClassY-
Appears in Collections:
Ochang Branch Institute > Division of Bioinfrastructure > Futuristic Animal Resource & Research Center > 1. Journal Articles
Ochang Branch Institute > Division of Bioinfrastructure > National Primate Research Center > 1. Journal Articles
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