The expression of the adhesion molecules ICAM-1, VCAM-1, PECAM, and E-selectin in human atherosclerosis
Article first published online: 15 JUN 2005
Copyright © 1993 John Wiley & Sons, Ltd.
The Journal of Pathology
Volume 171, Issue 3, pages 223–229, November 1993
How to Cite
Davies, M. J., Gordon, J. L., Gearing, A. J. H., Pigott, R., Woolf, N., Katz, D. and Kyriakopoulos, A. (1993), The expression of the adhesion molecules ICAM-1, VCAM-1, PECAM, and E-selectin in human atherosclerosis. J. Pathol., 171: 223–229. doi: 10.1002/path.1711710311
- Issue published online: 15 JUN 2005
- Article first published online: 15 JUN 2005
- Manuscript Accepted: 14 JUL 1993
- Manuscript Received: 15 APR 1993
The expression of PECAM, ICAM-1, VCAM-1, and E-selectin was studied in 64 samples of human coronary arteries taken from 15 explanted hearts obtained within 5 min of transplantation. Normal artery (n=12), predominantly fibrous plaques (n=23), and plaques containing extracellular lipid (n=26) and three segments showing recanalization channels were studied. All endothelial cells strongly and equally expressed PECAM; positive staining was used to check that artefactual denudation of the endothelial surface had not occurred. PECAM was also present in some lipid-filled macrophages. Normal arteries showed no VCAM-1 staining but focal segments of the endothelium were positive for ICAM-1 and E-selectin. ICAM-1 was strongly and constantly expressed by the endothelium over all types of plaques and in macrophages. E-selectin expression was confined to endothelial cells and occurred on the surface in 35 per cent of fibrous and 22 per cent of lipid-containing plaques. VCAM-1 staining of surface endothelium occurred in 39 per cent of fibrous and 20 per cent of lipid-containing plaques. A population of spindle-shaped cells of macrophage type (positive for EMB11 antigen) expressed VCAM-1 in lipid-containing plaques. Adventitial vessels adjacent to plaques showed endothelial expression of ICAM-1 and E-selectin. VCAM-1 staining of adventitial vessel endothelium was associated with local lymphoid aggregation. In conclusion, the expression of cell adhesion molecules is an important element in the inflammatory component of atherosclerosis and contributes to both monocyte and lymphocyte activation and recruitment from advential vessels and the arterial lumen.