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Volume 17, Number 8,
Issue of April 15, 1997
pp. 2746-2755
Copyright ©1997 Society for Neuroscience
Cyclo-Oxygenase-2 Gene Expression in Neurons Contributes to
Ischemic Brain Damage
Received Oct. 11, 1996; revised Feb. 3, 1997; accepted Feb. 6, 1997.
Shigeru Nogawa,
Fangyi Zhang,
M. Elizabeth Ross, and
Costantino Iadecola
Laboratory of Cerebrovascular Biology and Stroke, Department of
Neurology, University of Minnesota Medical School, Minneapolis,
Minnesota 55455
Cyclo-oxygenase-2 (COX-2), a rate-limiting enzyme for prostanoid
synthesis, is induced during inflammation and participates in
inflammation-mediated cytotoxicity. Cerebral ischemia is followed by an
inflammatory reaction that plays a role in the evolution of the tissue
damage. We studied whether COX-2 is induced after cerebral ischemia and
if so, whether such expression contributes to ischemic brain damage.
The middle cerebral artery was occluded in rats, and the ischemic area
was sampled for analysis 3-96 hr later. COX-2 mRNA was determined by
the competitive reverse-transcription PCR. COX-2 mRNA was upregulated
in the ischemic hemisphere, but not contralaterally, beginning 6 hr
after ischemia. The upregulation reached a maximum at 12 hr, at which
time a fivefold induction of the message occurred. Twenty-four hours
after ischemia, the concentration of prostaglandin E2 was
elevated in the injured brain by 292 ± 57%
(n = 6). COX-2 immunoreactivity was observed in
neurons at the medial edge of the ischemic area. Administration of the
COX-2 inhibitor NS-398 attenuated the elevation in prostaglandin E2 in the postischemic brain and reduced the volume of the
infarct by 29 ± 6% (p < 0.05). Thus,
cerebral ischemia leads to upregulation of COX-2 message, protein, and
reaction products in the injured hemisphere. The data implicate COX-2
in the mechanisms of delayed neuronal death at the infarct border and
provide the rationale for neuroprotective strategies employing COX-2
inhibitors.
Key words:
stroke;
prostanoids;
prostaglandin H2
synthase;
gene expression;
NS-398;
reverse-transcription polymerase
chain reaction;
iNOS;
inflammation
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[Abstract]
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D. A. Kniss
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Reproductive Sciences,
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