The expression of the adhesion molecules ICAM‐1, VCAM‐1, PECAM, and E‐selectin in human atherosclerosis

Abstract

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 adventitial vessels and the arterial lumen.

Laser capture microdissection analysis of gene expression in macrophages from atherosclerotic lesions of apolipoprotein E-deficient mice

“…3). These three genes were chosen for study because their products are implicated in atherogenesis, as reflected by being upregulated in human coronary plaque (27)(28)(29) and in lesions of animal models of atherosclerosis (18,30,31). More direct support for causative roles has come from recent mouse studies.…”

Circulating intercellular cell adhesion molecule-1, endothelin-1 and von Willebrand factor-markers of endothelial dysfunction in uncomplicated essential hypertension: the effect of treatment with ACE inhibitors

“…2 Increased expression of cell adhesion molecules ICAM-1, VCAM-1 and E-selectin has been observed in human atherosclerotic plaques. 3,4 Furthermore, the amount of soluble ICAM-1 and E-selectin released into the circulation has been demonstrated to directly correlate with the surface expression of ICAM-1 and E-selectin in a culture of endothelial cells. 5 Upregulation of adhesion molecule genes leads to the expression of membraneassociated adhesion molecules and release of their soluble forms.…”

Detection of monocyte-derived microparticles in patients with Type II diabetes mellitus

“…E-selectin is a cell adhesion molecule that contributes to monocyte adhesion to endothelium [29] and is expressed by endothelial cells at the site of atheroscrelotic lesions [30]. Serum concentrations of soluble E-selectin (sE-selectin) are higher in patients with diabetes mellitus [9±11].…”