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학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
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Department of Neurology, Seoul National University; Neuroscience Research Institute, SNUMRC and ClinicalResearch Institute, Seoul National University Hospital, Seoul.
Background: HSP70 protein in mice, which is produced from two genes, hsp70.1 and hsp70.3, is known to pro-tect the brain against ischemic injury. However, little information is available on the anti-apoptotic mechanism ofHSP70.1 protein after cerebral ischemia. To evaluate the role of HSP70.1 in ischemia, we analyzed cytochrome crelease and nuclear fragmentation using hsp70.1 knock-out (KO) mice and their wild-type (WT) mice. Methods:hsp70.1 KO and WT mice underwent focal ischemia for 120 minutes. Morphological analysis was performed byNissl staining and Hoechst 33342 staining. HSP70 expression and cytochrome c release were analyzed by Westernblotting and immunohistochemistry.Reseults: Following focal ischemia, HSP70 protein expression was markedlysuppressed in KO mice versus WT mice. KO mice showed a significantly greater infarction volume and nuclearfragmentation in the cortex than WT mice at 24 hours after ischemia. At 8 hours, cytochrome c release into thecytosol was markedly higher in KO mice than in WT mice. Conclusions: These findings suggest that the deletionof the hsp70.1 gene increases cytochrome c release into the cytosol, thereby exacerbating apoptosis after focalcerebral ischemia.
대한뇌졸중학회지제6권제1호2004년5월
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