Time course of ICAM-1 expression and leukocyte subset infiltration in rat forebrain ischemia |
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Authors: | Wayne M Clark Jeffrey D Lauten Nikola Lessov William Woodward and Bruce M Coull |
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Institution: | (1) Oregon Stroke Center, Department of Neurology L104, Oregon Health Sciences University, 3181 SW Sam Jackson Pike Rd, 97201 Portland, OR;(2) Department of Neurology, Veterans Administration Medical Center, Portland, OR |
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Abstract: | The time course of ICAM-1 expression and leukocyte subset infiltration was studied in a model of CNS reperfusion injury in
adult rats. Leukocyte adhesion and infiltration, mediated in part by intercellular adhesion molecule-1 (ICAM-1), appears to
potentiate CNS reperfusion injury. The timing and relationship between ICAM-1 staining and leukocyte infiltration postglobal
CNS ischemia is unknown. Reversible forebrain ischemia was produced in 32 adult Sprague-Dawley rats using the two-vessel occlusion
model with histologic analysis performed at specific intervals postischemia: 1, 3, 6, 12 and 24h, 4 and 7 d, or sham-operated
controls (n=4 each group). Monoclonal antibodies against ICAM-1 (1A29 and TM8), a specific granulocyte (PMN) (HIS48), and a specific
monocyte/macrophage (M?)(ED1) were used. No specific leukocyte and only rare ICAM-1 vessel immunoreactivity was observed in
sham controls. ICAM-1: Significant expression in microvessels beginning at 1 h with additional diffuse CA1 pyramidal layer
staining beginning at 4 d. Leukocytes: NO PMN cells and rare M? identified at 6 and 12 h. By 24 h: moderate infiltrate in
areas of ICAM-1 expression of PMN and M?. At 4 and 7 d: only M? accumulation, cellular morphology now similar to microglia.
The results of this study indicate that early and persistent ICAM-1 expression occurs following CNS ischemia with associated
leukocyte infiltration. |
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Keywords: | ICAM-1 cerebral ischemia reperfusion injury leukocytes microglia macrophage |
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