Increased expression of intercellular adhesion molecule-1 in mouse focal cerebral ischemia model

Citation
Hl. Ge et al., Increased expression of intercellular adhesion molecule-1 in mouse focal cerebral ischemia model, CHIN MED J, 113(1), 2000, pp. 75-79
Citations number
10
Categorie Soggetti
General & Internal Medicine
Journal title
CHINESE MEDICAL JOURNAL
ISSN journal
03666999 → ACNP
Volume
113
Issue
1
Year of publication
2000
Pages
75 - 79
Database
ISI
SICI code
0366-6999(200001)113:1<75:IEOIAM>2.0.ZU;2-0
Abstract
Objective To quantitatively measure the temporal profiles of intercellular adhesion molecule-1 (ICAM-1) protein in mouse brain after middle cerebral a rtery occlusion (MCAO). Methods Adult male CD-1 mice received 0, 3, 6, 12, 24, 48 and 72 hour(s) of permanent MCAO with an intraluminal suture technique. The degree and the e xtent of occlusion were determined using a laser Doppler flowmeter. ICAM-1 positive expression in ischemic regions was determined immunohistochemicall y and ICAM-1 protein was quantitatively measured using immunoprecipitation and Western blot analysis. Results After MCAO, surface cerebral blood flow (CBF) in the ischemic hemis phere decreased to 9% - 15% of the baseline in each time point of 7 to 8 an imals. There were no significant differences in CBF measurement during occl usion between groups. Immunohistochemistry showed that ICAM-1 positive micr ovascular endothelial cells were observed both in the ischemic core and in the perifocal region. There was a tendency for increasing expression of ICA M-1 positive microvascular endothelial cells from the ischemic core to the ischemic margin. Western blot analysis showed that ICAM-1 expression in the ischemic hemisphere began to increase 3 h after MCAO, peaked at 6 h to 12 h, and persisted to 72 h. Conclusions ICAM-1 expression increases in mice with permanent MCAO because ICAM-1 can mediate leukocyte-endothelial adhesion and progression of leuko cyte infiltration after permanent focal cerebral ischemia. ICAM-1 is one of the important factors participating in ischemic cerebral damage and pathog enesis of stroke.