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Intercellular adhesion molecule‐1‐deficient mice are less susceptible to cerebral ischemia‐reperfusion lnjury
Author(s) -
Soriano Sulpicio G.,
Lipton Stuart A.,
Wang Yanming F.,
Xaio Min,
Springer Timothy A.,
GutierrezRamos JoseCarlos,
Hickey Paul R.
Publication year - 1996
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410390511
Subject(s) - intercellular adhesion molecule 1 , intracellular , ischemia , adhesion , cell adhesion molecule , reperfusion injury , medicine , microbiology and biotechnology , chemistry , biology , organic chemistry
Neutrophil emigration is mediated by adhesion proteins that are highly expressed on the endothelial surface during inflammatory processes in the brain. Intercellular adhesion molecule‐1 (ICAM‐1) is an inducible adhesion molecule that binds to leukocyte integrins and facilitates neutrophil adhesion and transendothelial migration. To study the role of ICAM‐1 during ischemia and reperfusion in the brain, we analyzed the effect of transient focal cerebral ischemia in ICAM‐1‐deficient mice generated by gene targeting in embryonic stem cells. Transient focal ischemia was induced by occluding the left middle cerebral artery for 3 hours followed by a 21‐ or 45‐hour reperfusion period. When compared with their wild‐type littermates, ICAM‐1‐deficient mice were less susceptible to cerebral injury as demonstrated by a 5.6‐ or 7.8‐fold reduction in infarction volume, respectively. These data support the premise that neutrophil adhesion in ischemic areas may be deleterious and that ICAM‐1 deficiency reduces neurological damage after transient focal cerebral ischemia.