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The temporal profiles of ICAM-1 protein and mRNA expression after transient MCA occlusion in the rat
Abstract:
Leukocytes may contribute to ischemic cell damage. ICAM-1 expression on endothelial cells facilitates the migration of leukocytes into tissue. Therefore, we measured the temporal profiles of ICAM-1 mRNA and protein in rat brain after transient (1 or 2 h) of middle cerebral artery (MCA) occlusion. Male Wistar rats (n = 86) were subjected to 1 or 2 h MCA of occlusion, or 2 h of MCA occlusion followed by reperfusion for a variety of durations ranging from 1 h to 1 week. 10 additional control animals were employed. ICAM-1 mRNA and protein were measured during ischemia and reperfusion, and immunohistochemical methods were used to identify specific cell types expressing ICAM-1. ICAM-1 mRNA was detected 1 h after the onset of ischemia. mRNA maximized at 10 h of reperfusion and persisted out to 1 week of reperfusion. ICAM-1 significantly increased in microvascular endothelial cells at 2 h of reperfusion, maximized at 46 h and persisted out to 1 week of reperfusion (P < 0.05). ICAM-1 mRNA and protein are present in ischemic brain early after the onset of ischemia and reperfusion, respectively. These data provide support for the role of ICAM-1 in mediating leukocyte-endothelial adhesion after transient MCA occlusion in the rat.
Insights
Leukocyte infiltration contributes to ischemic brain damage. Intercellular Adhesion Molecule-1 (ICAM-1) expression increases early in the brain after transient middle cerebral artery occlusion, supporting its role in leukocyte adhesion.
Area of Science:
- Neuroscience
- Immunology
- Pathology
Background:
- Leukocytes contribute to ischemic cell damage.
- Intercellular Adhesion Molecule-1 (ICAM-1) expression on endothelial cells facilitates leukocyte migration into tissues.
Purpose of the Study:
- To measure the temporal profiles of ICAM-1 mRNA and protein in rat brain following transient middle cerebral artery (MCA) occlusion.
- To investigate the role of ICAM-1 in mediating leukocyte-endothelial adhesion after ischemic stroke.
Main Methods:
- Male Wistar rats underwent 1 or 2 hours of MCA occlusion, with varying reperfusion durations.
- ICAM-1 mRNA and protein levels were quantified using immunohistochemical methods during ischemia and reperfusion.
- Specific cell types expressing ICAM-1 were identified.
Main Results:
- ICAM-1 mRNA was detected 1 hour after ischemia onset, peaking at 10 hours of reperfusion and persisting for 1 week.
- ICAM-1 protein significantly increased in microvascular endothelial cells by 2 hours of reperfusion, peaking at 46 hours and persisting for 1 week.
- Both ICAM-1 mRNA and protein were present in the ischemic brain early after ischemia and reperfusion.
Conclusions:
- ICAM-1 mRNA and protein are upregulated early in the ischemic brain after transient MCA occlusion.
- These findings support a role for ICAM-1 in leukocyte-endothelial cell adhesion during the inflammatory response to ischemic stroke.