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From the * Laboratory of Immunology and Vascular Biology, Department of Pathology, Stanford
University, Stanford, California 94305, and Center for Molecular Biology and Medicine, Veterans
Affairs Health Care System, Palo Alto, California 94304; Adhesion of monocytes to the endothelium in lesion-prone areas is one of the earliest events in
fatty streak formation leading to atherogenesis. The molecular basis of increased monocyte adhesion is not fully characterized. We have identified a novel vascular monocyte adhesion-associated protein, VMAP-1, that plays a role in adhesion of monocytes to activated endothelium.
Originally selected for its ability to block binding of a mouse monocyte-like cell line
(WEHI78/24) to cytokine- or LPS-stimulated cultured mouse endothelial cells in vitro, antiVMAP-1 mAb LM151 cross-reacts with rabbit endothelium and blocks binding of human
monocytes to cultured rabbit aortic endothelial cells stimulated with minimally modified low
density lipoprotein, thought to be a physiologically relevant atherogenic stimulus. Most importantly, LM151 prevents adhesion of normal monocytes and monocytoid cells to intact aortic endothelium from cholesterol-fed rabbits in an ex vivo assay. VMAP-1 is a 50-kD protein. Immunohistology of vessels reveals focal constitutive expression in aorta and other large vessels. VMAP-1 is thus a novel vascular adhesion-associated protein that appears to play a critical role
in monocyte adhesion to aortic endothelial cells in atherogenesis in vivo.
Department of Cardiovascular Medicine,
Stanford University, Stanford, California 94305; § Department of Pathology, Center for the Health
Sciences, University of California at Los Angeles, Los Angeles, California 90024
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