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J. Exp. Med.,
Volume 189, Number 4, February 15, 1999 719-727
By
From the * Department of Neurology, University of Minnesota, Minneapolis, Minnesota 55455; and
the The transcription factor interferon regulatory factor 1 (IRF-1) is involved in the molecular
mechanisms of inflammation and apoptosis, processes that contribute to ischemic brain injury. In this study, the induction of IRF-1 in response to cerebral ischemia and its role in ischemic
brain injury were investigated. IRF-1 gene expression was markedly upregulated within 12 h
of occlusion of the middle cerebral artery in C57BL/6 mice. The expression reached a peak 4 d
after ischemia (6.0 ± 1.8-fold; P < 0.001) and was restricted to the ischemic regions of the
brain. The volume of ischemic injury was reduced by 23 ± 3% in IRF-1+/ Department of Microbiology and Immunology, Uniformed Services University of the Health
Sciences, Bethesda, Maryland 20814
and by 46 ± 9%
in IRF-1/ mice (P < 0.05). The reduction in infarct volume was paralleled by a substantial
attenuation in neurological deficits. Thus, IRF-1 is the first nuclear transacting factor demonstrated to contribute directly to cerebral ischemic damage and may be a novel therapeutic target
in ischemic stroke.
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