Kynurenic acid attenuates MPP+-induced dopaminergic neuronal cell death via a Bax-mediated mitochondrial pathway

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dc.contributor.authorD Y Lee-
dc.contributor.authorKyu-Sun Lee-
dc.contributor.authorH J Lee-
dc.contributor.authorY H Noh-
dc.contributor.authorD H Kim-
dc.contributor.authorJ Y Lee-
dc.contributor.authorS H Cho-
dc.contributor.authorO J Yoon-
dc.contributor.authorW B Lee-
dc.contributor.authorK Y Kim-
dc.contributor.authorY H Chung-
dc.contributor.authorS S Kim-
dc.date.accessioned2017-04-19T09:10:19Z-
dc.date.available2017-04-19T09:10:19Z-
dc.date.issued2008-
dc.identifier.issn0171-9335-
dc.identifier.uri10.1016/j.ejcb.2008.03.003ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/8450-
dc.description.abstractKynurenic acid (KYNA), a tryptophan metabolite in the kynurenine pathway, is protective against various insults. However, the molecular mechanism of this protective effect has not been identified. In this study, we examined the protective effects of KYNA against 1-methyl-4-phenylpyridinium (MPP+), the best-characterized toxin inducing pathological changes resembling Parkinson's disease (PD), using SH-SY5Y and SK-N-SH human neuroblastoma cells. Pre-treatment of KYNA attenuated MPP+-induced neuronal cell death in SH-SY5Y and SK-N-SH cells. MPP+-induced cell death was preceded by increases in Bax expression and mitochondrial dysfunction, such as collapse of mitochondrial membrane potential (ΔΨm), release of cytochrome c from mitochondria into the cytoplasm, and increases in caspase-9/-3 activities. KYNA effectively inhibited all of these mitochondrial apoptotic processes. Our results indicate that KYNA plays a protective role by down-regulating Bax expression and maintaining mitochondrial function in MPP+-induced neuronal cell death, and suggest that KYNA may have therapeutic potential in PD.-
dc.publisherElsevier-
dc.titleKynurenic acid attenuates MPP+-induced dopaminergic neuronal cell death via a Bax-mediated mitochondrial pathway-
dc.title.alternativeKynurenic acid attenuates MPP+-induced dopaminergic neuronal cell death via a Bax-mediated mitochondrial pathway-
dc.typeArticle-
dc.citation.titleEuropean Journal of Cell Biology-
dc.citation.number6-
dc.citation.endPage397-
dc.citation.startPage389-
dc.citation.volume87-
dc.contributor.affiliatedAuthorKyu-Sun Lee-
dc.contributor.alternativeName이도연-
dc.contributor.alternativeName이규선-
dc.contributor.alternativeName이현정-
dc.contributor.alternativeName노유훈-
dc.contributor.alternativeName김도희-
dc.contributor.alternativeName이준영-
dc.contributor.alternativeName조수현-
dc.contributor.alternativeName윤옥자-
dc.contributor.alternativeName이원복-
dc.contributor.alternativeName김경용-
dc.contributor.alternativeName정윤희-
dc.contributor.alternativeName김성수-
dc.identifier.bibliographicCitationEuropean Journal of Cell Biology, vol. 87, no. 6, pp. 389-397-
dc.identifier.doi10.1016/j.ejcb.2008.03.003-
dc.subject.keyword1-methyl-4-phenylpyridinium (MPP+)-
dc.subject.keywordBax-
dc.subject.keywordKynurenic acid (KYNA)-
dc.subject.keywordMitochondrial dysfunction-
dc.subject.keywordNeuronal apoptosis-
dc.subject.local1-methyl-4-phenylpyridinium (MPP+)-
dc.subject.localBax-
dc.subject.localbax-
dc.subject.localKynurenic acid (KYNA)-
dc.subject.localMitochondrial dysfunction-
dc.subject.localmitochondrial dysfunction-
dc.subject.localMitochondrial Dysfunction-
dc.subject.localNeuronal apoptosis-
dc.description.journalClassY-
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