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Apoptosis and Necrosis in Cerebrovascular Disease
Author(s) -
SNIDER B. JOY,
GOTTRON FRANK J.,
CHOI DENNIS W.
Publication year - 1999
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.1999.tb07829.x
Subject(s) - apoptosis , cycloheximide , programmed cell death , necrosis , tunel assay , ischemia , dna fragmentation , biology , in vivo , glutamate receptor , pathology , medicine , cell culture , receptor , biochemistry , genetics
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 bax gene. Neurons may undergo both apoptosis and necrosis after ischemic insults, and thus it may be therapeutically desirable to block both processes.