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ICAM-1 expression on human brain microvascular endothelial cells
D C Hess1, T Bhutwala, J C Sheppard
1Neurology Service, Veterans Affairs Medical Center, Augusta, GA 30904.
Neuroscience Letters
|February 28, 1994
Summary
Leukocyte migration into the brain during ischemic stroke is mediated by intercellular adhesion molecule-1 (ICAM-1). Brain endothelial cells show greater ICAM-1 upregulation than umbilical vein cells when stimulated, and dexamethasone did not inhibit this response.
Area of Science:
- Neuroscience
- Immunology
- Cell Biology
Background:
- Leukocytes contribute to tissue damage in acute ischemic stroke.
- Intercellular adhesion molecule-1 (ICAM-1) is crucial for leukocyte migration into the brain.
Purpose of the Study:
- To compare ICAM-1 expression in human brain microvascular endothelial cells (HBMECs) versus human umbilical vein endothelial cells (HUVECs).
- To investigate the effect of cytokine or lipopolysaccharide stimulation on ICAM-1 expression.
- To evaluate the inhibitory effect of dexamethasone on ICAM-1 upregulation.
Main Methods:
- Enzyme-linked immunosorbent assay (ELISA) was used to quantify ICAM-1 expression.
- HBMECs and HUVECs were stimulated with cytokines (IL-1β, TNF) or lipopolysaccharide.
- Cells were treated with varying concentrations of dexamethasone.
Main Results:
- Constitutive surface expression of ICAM-1 was observed on both HBMECs and HUVECs.
- Cytokine or lipopolysaccharide stimulation resulted in a greater increase in ICAM-1 expression on HBMECs compared to HUVECs.
- Dexamethasone, up to 100 μM, did not inhibit cytokine-mediated ICAM-1 upregulation on HBMECs.
Conclusions:
- HBMECs exhibit a heightened response in ICAM-1 expression compared to HUVECs upon stimulation.
- The findings suggest specific endothelial cell responses in the brain relevant to ischemic stroke pathophysiology.
- Dexamethasone is ineffective in modulating ICAM-1 upregulation in this context, indicating potential limitations for its use in mitigating stroke-related inflammation via this pathway.