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Volume 17, Number 23,
Issue of December 1, 1997
pp. 9157-9164
Delayed Reduction of Ischemic Brain Injury and Neurological
Deficits in Mice Lacking the Inducible Nitric Oxide Synthase Gene
Received Aug. 4, 1997; revised Sept. 18, 1997; accepted Sept. 18, 1997.
Costantino Iadecola,
Fangyi Zhang,
Robyn Casey,
Masao Nagayama, and
M. Elizabeth Ross
Department of Neurology, University of Minnesota, Minneapolis,
Minnesota 55455
Inducible nitric oxide synthase (iNOS), an enzyme that produces
toxic amounts of nitric oxide, is expressed in a number of brain
pathologies, including cerebral ischemia. We used mice with a null
mutation of the iNOS gene to study the role of iNOS in ischemic brain
damage. Focal cerebral ischemia was produced by occlusion of the middle
cerebral artery (MCA). In wild-type mice, iNOS mRNA expression in the
post-ischemic brain begun between 24 and 48 hr peaked at 96 hr and
subsided 7 d after MCA occlusion. iNOS mRNA induction was
associated with expression of iNOS protein and enzymatic activity. In
contrast, mice lacking the iNOS gene did not express iNOS message or
protein after MCA occlusion. The infarct and the motor deficits
produced by MCA occlusion were smaller in iNOS knockouts than in
wild-type mice (p < 0.05). Such reduction
in ischemic damage and neurological deficits was observed 96 hr after
ischemia but not at 24 hr, when iNOS is not yet expressed in wild-type
mice. The decreased susceptibility to cerebral ischemia in iNOS
knockouts could not be attributed to differences in the degree of
ischemia or vascular reactivity between wild-type and knockout mice.
These findings indicate that iNOS expression is one of the factors
contributing to the expansion of the brain damage that occurs in the
post-ischemic period. iNOS inhibition may provide a novel therapeutic
strategy targeted specifically at the secondary progression of ischemic
brain injury.
Key words:
cerebral ischemia;
knockout mice;
gene expression;
neuroprotection;
stroke;
reverse-transcription PCR
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D. O'MAHONY and M. J KENDALL
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D. J. Lefer, S. P. Jones, W. G. Girod, A. Baines, M. B. Grisham, A. S. Cockrell, P. L. Huang, and R. Scalia
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