期刊
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM
卷 21, 期 12, 页码 1411-1421出版社
SAGE PUBLICATIONS INC
DOI: 10.1097/00004647-200112000-00005
关键词
apoptosis; caspase; Fas; Fas-L; FADD; ischemia
资金
- NINDS NIH HHS [NS35965] Funding Source: Medline
Cell death-regulatory genes like caspases and bcl-2 family genes are involved in delayed cell death in the CAI sector of hippocampus after global cerebral ischemia, but little is known about the mechanisms that trigger their expression. The authors found that expression of Fas and Fas-ligand messenger ribonucleic acid and protein was induced in vulnerable CA1 neurons at 24 and 72 hours after global ischemia. Fas-associating protein with a novel death domain (FADD) also was upregulated and immunoprecipitated and co-localized with Fas. Caspase-10 was activated and interacted with FADD protein to an increasing extent as the duration of ischemia increased. Moreover, caspase-10 co-localized with both FADD and caspase-3. These findings suggest that Fas-mediated death signaling may play an important role in signaling hippocampal neuronal death in CA1 after global cerebral ischemia.
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