Journal
EUROPEAN SURGICAL RESEARCH
Volume 34, Issue 1-2, Pages 37-41Publisher
KARGER
DOI: 10.1159/000048885
Keywords
cerebral ischemia; apoptotic cell death; cytochrome c release; BID; knock-out mice
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Funding
- NINDS NIH HHS [NS10828, NS374141-02] Funding Source: Medline
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [P50NS010828, P01NS010828] Funding Source: NIH RePORTER
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Mitochondrial mechanisms, particularly the release of cytochrome c, play a role in the death of nerve and glial cells in cerebral ischemia. We have currently investigated whether BID, a proapoptotic molecule of the bcl-2 family and promoter of the release of cytochrome c is expressed in the brain, activated by cerebral ischemia in vivo, and contributes to ischemic cell death. We found BID in the cytosol of mouse brain and of primary cultured mouse neurons and showed that neuronal BID is a substrate for caspase 8. BID was cleaved in vivo 4 h after transitory occlusion of the middle cerebral artery. Further, BID-/- mice had a significant attenuation of infarction (-67%) and significantly lower release of cytochrome c (-41 %). The findings indicate that the proapoptotic molecule BID may contribute to the demise of nerve cells from cerebral ischemia by release of cytochrome c and activation of caspase. Copyright (C) 2002 S. Karger AG, Basel.
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