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The transcription factor interferon regulatory factor 1 is expressed after cerebral ischemia and contributes to ischemic brain injury.

作者信息

Iadecola C, Salkowski C A, Zhang F, Aber T, Nagayama M, Vogel S N, Ross M E

机构信息

Department of Neurology, University of Minnesota, Minneapolis, Minnesota 55455, USA.

出版信息

J Exp Med. 1999 Feb 15;189(4):719-27. doi: 10.1084/jem.189.4.719.

DOI:10.1084/jem.189.4.719
PMID:9989987
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2192924/
Abstract

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.

摘要
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/facb/2192924/ce7c9974b6b4/JEM981844.f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/facb/2192924/70bd02d38991/JEM981844.f1a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/facb/2192924/604ad018f859/JEM981844.f2a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/facb/2192924/d11cb1cb06a2/JEM981844.f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/facb/2192924/63c8b3220b3a/JEM981844.f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/facb/2192924/dd091d2cb64f/JEM981844.f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/facb/2192924/ce7c9974b6b4/JEM981844.f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/facb/2192924/70bd02d38991/JEM981844.f1a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/facb/2192924/604ad018f859/JEM981844.f2a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/facb/2192924/d11cb1cb06a2/JEM981844.f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/facb/2192924/63c8b3220b3a/JEM981844.f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/facb/2192924/dd091d2cb64f/JEM981844.f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/facb/2192924/ce7c9974b6b4/JEM981844.f6.jpg

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Protein kinase C expression and activity after global incomplete cerebral ischemia in dogs.
Nat Neurosci. 2023 Dec;26(12):2042-2045. doi: 10.1038/s41593-023-01505-2.
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Role of Na/K-ATPase in ischemic stroke: in-depth perspectives from physiology to pharmacology.钠钾ATP酶在缺血性卒中中的作用：从生理学到药理学的深入见解
J Mol Med (Berl). 2022 Mar;100(3):395-410. doi: 10.1007/s00109-021-02143-6. Epub 2021 Nov 27.
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