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Endothelial cell integrin laminin receptor expression in multiple sclerosis lesions
R A Sobel1, J R Hinojoza, A Maeda
1Pathology Service, Veterans Affairs Health Care System, Palo Alto, California 94304, USA.
The American Journal of Pathology
|August 26, 1998
Summary
Integrin receptors on endothelial cells change in multiple sclerosis (MS) lesions. Decreased beta1/VLA-6 integrins in active MS lesions may cause blood-brain barrier breakdown, while increased VLA-1 may indicate dysfunction.
Area of Science:
- Neuroimmunology
- Cellular Biology
- Vascular Biology
Background:
- Laminin, a key basement membrane glycoprotein, interacts with endothelial cell integrins (beta1 and beta3).
- Integrin function in multiple sclerosis (MS) lesions is not fully understood.
Purpose of the Study:
- To investigate the expression and localization of endothelial cell integrin laminin receptors in central nervous system samples from MS patients and controls.
- To determine the role of specific integrins in different stages of MS lesions.
Main Methods:
- Immunohistochemistry was used to analyze integrin laminin receptors and laminin in MS and control CNS samples.
- Immunoelectron microscopy was employed to determine the subcellular distribution of integrins and laminin.
Main Results:
- Active MS lesions showed decreased endothelial cell VLA-6 and beta1 subunits, but increased alpha(v) and VLA-1.
- Chronic inactive lesions had normalized beta1 and VLA-6, but persistently elevated VLA-1.
- Integrins and laminin showed distinct cellular localizations, including luminal surfaces and intercellular junctions.
Conclusions:
- Distinct integrin regulation occurs during different MS lesion stages.
- Decreased beta1/VLA-6 in active lesions may contribute to leukocyte migration and blood-brain barrier breakdown.
- Increased VLA-1 in chronic lesions suggests ongoing endothelial cell dysfunction and blood-brain barrier impairment.