Mj. Davies et al., THE EXPRESSION OF THE ADHESION MOLECULES ICAM-1, VCAM-1, PECAM, AND E-SELECTIN IN HUMAN ATHEROSCLEROSIS, Journal of pathology, 171(3), 1993, pp. 223-229
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), predom
inantly fibrous plaques (n=23), and plaques containing extracellular l
ipid (n=26) and three segments showing recanalization channels were st
udied. All endothelial cells strongly and equally expressed PECAM; pos
itive staining was used to check that artefactual denudation of the en
dothelial surface had not occurred. PECAM was also present in some lip
id-filled macrophages. Normal arteries showed no VCAM-1 staining but f
ocal segments of the endothelium were positive for ICAM-1 and E-select
in. ICAM-1 was strongly and constantly expressed by the endothelium ov
er all types of plaques and in macrophages. E-selectin expression was
confined to endothelial cells and occurred on the surface in 35 per ce
nt of fibrous and 22 per cent of lipid-containing plaques. VCAM-I stai
ning of surface endothelium occurred in 39 per cent of fibrous and 20
per cent of lipid-containing plaques. A population of spindle-shaped c
ells of macrophage type (positive for EMB11 antigen) expressed VCAM-1
in lipid-containing plaques. Adventitial vessels adjacent to plaques s
howed 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 atheroscleros
is and contributes to both monocyte and lymphocyte activation and recr
uitment from advential vessels and the arterial lumen.