Low density lipoprotein binding to human platelets: role of charge and of specific amino acids.
ABSTRACT Many human and animal cells possess cell surface binding sites, specific for low density lipoproteins. Human platelets are similarly endowed with specific low density lipoprotein receptors. Using chemical modofications of amino acid residues on the low density lipoprotein molecule, we have studied the role of charge and specific amino acids on the binding process. The interaction of the modified low density lipoprotein preparations with gel-filtered platelets and with glass beads was compared. Both cyclohexanedione treated and aceto-acetylated low density lipoprotein did not bind to the platelet surface. However, azo-arsanilated low density lipoprotein bound to the platelets in a manner similar to the binding of native lipoprotein. Cyclohexanedione treated lipoprotein was the only preparation which did not bind to glass beads. The importance of both the presence of the positive charge on the lipoprotein molecule and the availability of specific amino acid residues (arginine and lysine but not tyrosine and histidine) for low density lipoprotein-platelet interaction was thus demonstrated.
- Doklady Biological Sciences 11/2013; 453(1):333-5.
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ABSTRACT: Although much emphasis has been placed on the role of cholesterol and lipoproteins in atherosclerotic plaque formation, recent studies suggest that lipids have other vascular actions which may contribute to the pathogenesis of myocardial ischemia. These include deleterious effects of lipids on platelet and endothelial cell function, coagulation, fibrinolysis, and prostacyclin metabolism. The purpose of this report is to review recent data regarding the nonatherogenic effects of lipids and provide insight as to how lipid lowering might contribute to clinically important improvements in vascular biology.Clinical Cardiology 02/2009; 15(12):883 - 890. · 1.83 Impact Factor
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ABSTRACT: In the last decade, it was recognized that platelets and lipoproteins play a pivotal role in both early and late atherogenesis. Beside cellular interactions of platelets with other blood cells and vascular cells, interactions with lipoproteins seem to be quite important. Lipoproteins are fundamental 'players' in atherogenesis since they change the properties of different cells involved in atherosclerosis and thrombosis. Several studies have already shown that low density lipoproteins (LDL) are involved in the initiation of platelet signalling pathways. Platelets of hypercholesterolemic patients show hyperaggregability in vitro and enhanced activity in vivo. This review elucidates the major aspects concerning how native and modified lipoproteins influence the activation and metabolic behaviour of platelets, and shows a new way by which platelet-mediated lipoprotein transfer might contribute to foam cell formation. In hyperlipidaemia, circulating platelets are activated. This is accompanied by increased platelet aggregation, platelet-leukocyte aggregate formation, and platelet-induced superoxide anion production. Furthermore, oxidized LDL induces monocyte adhesion to the endothelium, migration and proliferation of smooth muscle cells, injures cells, interferes with nitric oxide release, and promotes procoagulant properties of vascular cells. New data about platelet-mediated lipoprotein transport and consequent foam cell formation, however, provide proof of how platelets might contribute to atheromatous lesion formation.Cardiovascular Research 05/2008; 78(1):8-17. · 5.94 Impact Factor