Fas (CD95) may mediate delayed cell death in hippocampal CA1 sector after global cerebral ischemia

Kunlin Jin, Steven H. Graham, Xiaoou Mao, Tetsuya Nagayama, Roger P. Simon, David A. Greenberg

Research output: Contribution to journalArticle

68 Scopus citations

Abstract

Cell death-regulatory genes like caspases and bcl-2 family genes are involved in delayed cell death in the CA1 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.

Original languageEnglish
Pages (from-to)1411-1421
Number of pages11
JournalJournal of Cerebral Blood Flow and Metabolism
Volume21
Issue number12
DOIs
StatePublished - 1 Jan 2001

    Fingerprint

Keywords

  • Apoptosis
  • Caspase
  • FADD
  • Fas
  • Fas-L
  • Ischemia

Cite this