PARTIAL CHARACTERIZATION OF LEUKOCYTE BINDING-MOLECULES ON ENDOTHELIAL-CELLS INDUCED BY MINIMALLY OXIDIZED LDL

Treatment of rabbit aortic endothelial cells, human umbilical vein end othelial cells, and human aortic endothelial cells for 4 hours with mi nimally oxidized low-density lipoprotein (MM-LDL) induced the adhesion of monocytes but not neutrophils or lymphocytes to these cells. This induction was blocked by inhibitors of glycoprotein synthesis (cyclo-h eximide and tunicamycin), and binding was abolished by treatment of ce lls with low levels of trypsin, suggesting that the binding molecule(s ) is a protein. There was no increase in binding of antibodies to E-se lectin, vascular cell adhesion molecule-1 (VCAM-1), or intercellular a dhesion molecule-1 (ICAM-1) after treatment of cells with MM-LDL. Trea tment of endothelial cells with Fab fragments of antibody to monocyte chemotactic protein-1 or to fibronectin did not block monocyte binding . Several sugars (lactose-1-phosphate, maltose-1-phosphate, and N-acet ylglucosamine) inhibited monocyte binding to cells treated with MM-LDL , but binding was not blocked by mannose-6-phosphate, fructose-6-phosp hate, glucose-1-phosphate, or glucose-6-phosphate. EDTA or EGTA treatm ent inhibited binding, which was restored by adding either calcium or magnesium. We conclude that the binding of monocytes to endothelial ce lls induced by a 4-hour treatment with MM-LDL is caused by a binding m olecule(s) other than E-selectin, VCAM-1, or ICAM-1 and that carbohydr ate chains on the monocytes or the endothelium play a role in binding. (Arterioscler Thromb. 1994;14:427-433.)