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Volume 16, Number 13,
Issue of July 1, 1996
pp. 4146-4154
Copyright ©1996 Society for Neuroscience
Increased Expression of IL-1 Converting Enzyme in Hippocampus
after Ischemia: Selective Localization in Microglia
Received March 15, 1996; revised April 16, 1996; accepted April 18, 1996.
Ratan V. Bhat,
Richard DiRocco,
Val R. Marcy,
Dorothy
G. Flood,
Yuan Zhu,
Pawel Dobrzanski,
Robert Siman,
Richard Scott,
Patricia C. Contreras, and
Matthew Miller
Cephalon Incorporated, West Chester, Pennsylvania 19380
Although the interleukin-1 converting enzyme (ICE)/CED-3 family
of proteases has been implicated recently in neuronal cell death
in vitro and in ovo, the role of specific genes
belonging to this family in cell death in the nervous system remains
unknown. To address this question, we examined the in vivo
expression of one of these genes, Ice, after global
forebrain ischemia in gerbils. Using RT-PCR and Western immunoblot
techniques, we detected an increase in the mRNA and protein expression
of ICE in hippocampus during a period of 4 d after ischemia.
Chromatin condensation was observed in CA1 neurons within 2 d
after ischemia. Internucleosomal DNA fragmentation and apoptotic bodies
were observed between 3 and 4 d after ischemia, a period during
which CA1 neuronal death is maximal. In nonischemic brains, ICE-like
immunoreactivity was relatively low in CA1 pyramidal neurons but high
in scattered hippocampal interneurons. After ischemia, ICE-like
immunoreactivity was not altered in these neurons. ICE-like
immunoreactivity, however, was observed in microglial cells in the
regions adjacent to the CA1 layer as early as 2 d after ischemic
insult. The increase in ICE-like immunoreactivity was robust at 4 d after ischemia, a period that correlates with the DNA fragmentation
observed in hippocampal homogenates of ischemic brains. These results
provide the first evidence for the localization and induction of ICE
expression in vivo after ischemia and suggest an indirect
role for ICE in ischemic damage through mediation of an inflammatory
response.
Key words:
apoptosis;
interleukin-1 converting enzyme;
neuronal cell death;
global forebrain ischemia;
glia;
hippocampus
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