ABSTRACT
During atherosclerotic plaque development the adhesion molecule pathway is activated. Expressed adhesion molecules attract leukocytes to the endothelium (Fig. 2). Cells are attracted to the endothelial adhesion molecule receptors (a). Th e cells then ‘roll’ along the endothelium (b), become fi rmly attached to it (c) and migrate into the subintimal spaces (d), where they take up lipids to become foam cells and fatty plaques (Krieglstein and Granger 2001). Th e selectin family of adhesion molecules are involved in the adhesion of leukocytes to the activated endothelium and the observed cell ‘rolling’. Two diff erent adhesion molecules belonging to the Immunoglobulin (Ig) superfamily, ICAM-1 and vascular cell adhesion molecule 1 (VCAM-1), are involved in the extravasation of leukocytes into the surrounding tissue. Th e expressed endothelial adhesion molecules bind to their complementary ligands on the leukocytes, many of which belong to the integrin family. P-selectin is stored in specifi c granules that are present in platelets and endothelial cells from where it is mobilized to the cell surface aft er stimulation. E-selectin, however, is not stored, but increased surface expression can occur in response to transcription-dependent protein synthesis.
