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Department of Microbiology and Immunology, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814
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+/– 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.
Key Words: cerebral ischemia interferon regulatory factor 1 null mice gene expression neuroprotection reverse transcription polymerase chain reaction
The excellent editorial assistance of Ms. Karen MacEwan is acknowledged. We wish to thank Ms. Diana Miller for technical assistance.
Abbreviations used: CBF, cerebral blood flow; HPRT, hypoxanthine-guanine phosphoribosyl transferase; IRF-1, interferon regulatory factor 1, iNOS, inducible nitric oxide synthase; MCA, middle cerebral artery; NO, nitric oxide.
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