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영구적 국소 대뇌 허혈 생쥐 모델에서 활성 산소종에 의한 세포고사 유도인자의 핵내 이동과 세포고사

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dc.contributor.author김경환-
dc.contributor.author김현우-
dc.contributor.author이병인-
dc.contributor.author조상래-
dc.contributor.author조양제-
dc.date.accessioned2017-09-29T06:33:47Z-
dc.date.available2017-09-29T06:33:47Z-
dc.date.issued2005-
dc.identifier.issn1229-4101-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/149941-
dc.description.abstractBackground: Recently, the mitochondrial proapoptotic protein, apoptosis-inducing factor (AIF), and its nuclear translocation have been reported in caspase-independent neuronal apoptosis. However, it is not elucidated whether oxidative signaling is involved in the nuclear translocation of AIF and subsequent caspase-independent apoptotic cell death. We investigated whether oxidative signaling induces nuclear translocation of AIF and subsequent caspase- independent apoptosis-associated DNA fragmentation after permanent focal cerebral ischemia (FCI). Methods: Adult male ICR mice were subjected to permanent FCI by intraluminal suture blockade of middle cerebral artery. Immunohistochemistry and Western blot analysis were performed. Large-scale DNA fragmentation was evaluated by pulse field gel electrophoresis and apoptotic cell death was quantified. Manganese tetrakis (4-benzoic acid) porphyrin (MnTBAP), which mimics mitochondrial superoxide dismutase, was used to determinewhether the production of reactive oxygen species is required for the induction in AIF translocation. Results: Western blot analysis showed that the nuclear translocation of AIF occurred as early as 2 hours after permanent FCI. Immunostaining for AIF also confirmed early nuclear translocation of AIF after permanent FCI. Large-scale DNA fragmentation was detected 8 hours after permanent FCI. MnTBAP-treatment attenuated AIF translocation and blocked large-scale DNA fragmentation. Caspase-3 activity was similarly inhibited between the pan-caspase inhibitor- and MnTBAP-treated mice, but the amount of apoptosis-associated DNA fragmentation in the MnTBAP-treated mice was less than in the pan-caspase inhibitor-treated mice (P<0.001). In addition, infarction volume was also decreased by MnTBAP. Conclusions: These results suggest that reactive oxygen species induce the caspase-independent nuclear translocation of AIF and subsequent apoptosis-associated DNA fragmentation after permanent FCI.-
dc.description.statementOfResponsibilityopen-
dc.languageKorean-
dc.publisher대한뇌졸중학회-
dc.relation.isPartOfKorean Journal of Stroke (대한뇌졸중학회지)-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rightshttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHApoptosis-
dc.subject.MESHIschemic brain injury-
dc.subject.MESHOxidative stress-
dc.subject.MESHApoptosis-inducing factor-
dc.title영구적 국소 대뇌 허혈 생쥐 모델에서 활성 산소종에 의한 세포고사 유도인자의 핵내 이동과 세포고사-
dc.title.alternativeNuclear Translocation of Apoptosis Inducing Factor and Subsequent DNA Fragmentation by Reactive Oxygen Species After Permanent Focal Cerebral Ischemia in Mice-
dc.typeArticle-
dc.publisher.locationKorea-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Neurology (신경과학교실)-
dc.contributor.departmentYonsei Biomedical Research Center (연세의생명연구원)-
dc.contributor.departmentDept. of Neurology (신경과학교실)-
dc.contributor.departmentDept. of Microbiology (미생물학교실)-
dc.contributor.departmentDept. of Neurology (신경과학교실)-
dc.contributor.googleauthor조양제-
dc.contributor.googleauthor이용현-
dc.contributor.googleauthor조경주-
dc.contributor.googleauthor이두재-
dc.contributor.googleauthor김현우-
dc.contributor.googleauthor김현정-
dc.contributor.googleauthor이병인-
dc.contributor.googleauthor조상래-
dc.contributor.googleauthor김경환-
dc.identifier.doiOAK-2005-06528-
dc.contributor.localIdA00310-
dc.contributor.localIdA01125-
dc.contributor.localIdA02797-
dc.contributor.localIdA03824-
dc.contributor.localIdA03851-
dc.relation.journalcodeJ02121-
dc.relation.journalsince1999~2011-
dc.relation.journalafter2013~ Journal of Stroke-
dc.subject.keywordApoptosis-
dc.subject.keywordIschemic brain injury-
dc.subject.keywordOxidative stress-
dc.subject.keywordApoptosis-inducing factor-
dc.contributor.alternativeNameKim, Gyung Whan-
dc.contributor.alternativeNameKim, Hyun Woo-
dc.contributor.alternativeNameLee, Byung In-
dc.contributor.alternativeNameCho, Sang Nae-
dc.contributor.alternativeNameCho, Yang Je-
dc.citation.volume7-
dc.citation.number2-
dc.citation.startPage214-
dc.citation.endPage223-
dc.identifier.bibliographicCitationKorean Journal of Stroke (대한뇌졸중학회지), Vol.7(2) : 214-223, 2005-
dc.date.modified2017-05-04-
dc.identifier.rimsid42030-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Microbiology (미생물학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Neurology (신경과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Yonsei Biomedical Research Center (연세의생명연구원) > 1. Journal Papers

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