Intercellular adhesion molecule-1-deficient mice are less susceptible to cerebral ischemia-reperfusion injury.
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.
Soriano
S G
SG
Department of Anesthesia Children's Hospital, Boston, MA 02115, USA.
Lipton
S A
SA
Wang
Y F
YF
Xiao
M
M
Springer
T A
TA
Gutierrez-Ramos
J C
JC
Hickey
P R
PR
D000818:Animals; D015152:Blotting, Northern; D002540:Cerebral Cortex / Q000098:blood supply* / Q000378:metabolism / Q000473:pathology; D018799:Intercellular Adhesion Molecule-1 / Q000235:genetics* / Q000378:metabolism; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D012333:RNA, Messenger / Q000032:analysis; D015427:Reperfusion Injury / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D013997:Time Factors; D014158:Transcription, Genetic / Q000502:physiology
D012333:RNA, Messenger; D018799:Intercellular Adhesion Molecule-1