Michael A. Gimbrone

TL;DR: Endothelial leukocyte adhesion molecule-1 (ELAM-1), a cell surface glycoprotein expressed by cytokine-activated endothelium, mediates the adhesion of blood neutrophils and may be a member of a nascent gene family of cell surface molecules involved in the regulation of inflammatory and immunological events at the interface of vessel wall and blood.

TL;DR: This review traces the evolution of the concept of endothelial cell dysfunction, focusing on recent insights into the cellular and molecular mechanisms that underlie its pivotal roles in atherosclerotic lesion initiation and progression; explores its relationship to classic, as well as more recently defined, clinical risk factors for atherosclerosis.

TL;DR: It is proposed that nitric oxide's ability to limit endothelial activation and inhibit monocyte adhesion may contribute to some of its antiatherogenic and antiinflammatory properties within the vessel wall.

TL;DR: In dietary hypercholesterolemic and Watanabe heritable hyperlipidemic rabbit models of atherosclerosis, this inducible rabbit endothelial adhesion molecule was found to be expressed in a localized fashion by aortic endothelium that overlies early foam cell lesions, suggesting a potential endothelia-dependent mechanism for mononuclear leukocyte recruitment during atherogenesis.

TL;DR: Two monoclonal antibodies are developed that identify a cell-surface antigen expressed on cytokine- and endotoxin-stimulated H EC but not on unstimulated HEC that is designated "endothelial-leukocyte adhesion molecule-1 (ELAM-1)."