Apoptosis and necrosis in cerebrovascular disease

B. Joy Snider, Frank J. Gottron, Dennis W. Choi

Research output: Contribution to journalArticle

111 Scopus citations

Abstract

Neuronal death following ischemic insults has been thought to reflect necrosis. However, recent evidence from several labs suggests that programmed cell death, leading to apoptosis, might additionally contribute to this death. We have used both in vitro and in vivo models to study the role of apoptosis in ischemic cell death. Some features of apoptosis (TUNEL staining, internucleosomal DNA fragmentation, sensitivity to cycloheximide) were observed following transient focal ischemia in rats. Brief transient focal ischemia was followed by delayed infarction more than 3 days later; this delayed infarction was sensitive to cycloheximide. A cycloheximide-sensitive component of neuronal cell death was also observed in cultured murine neocortical neurons deprived of oxygen-glucose in the presence of glutamate receptor antagonists. This presumed ischemic apoptosis was attenuated by caspase inhibitors, or by homozygous deletion of the box gene. Neurons may undergo both apoptosis and necrosis after ischemic insults, and thus it may be therapeutically desirable to block both processes.

Original languageEnglish
Pages (from-to)243-253
Number of pages11
JournalAnnals of the New York Academy of Sciences
Volume893
DOIs
StatePublished - Jan 1 1999

Fingerprint Dive into the research topics of 'Apoptosis and necrosis in cerebrovascular disease'. Together they form a unique fingerprint.

  • Cite this