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.
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- FEBS Letters 02/1982; 137(2):319-22. DOI:10.1016/0014-5793(82)80375-X · 3.17 Impact Factor
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ABSTRACT: Using a platelet-rich plasma (PRP) preparation, platelets from subjects with familial hypercholesterolemia (FH) were found to be more reactive to the aggregating agents epinephrine, ADP and thrombin than platelets obtained from normal individuals. Gel-filtered platelets (GFP) i.e. platelets free of any plasma constituents also showed increased activation as determined by platelet aggregation and 14C-serotonin release. On incubating washed platelets from normal subjects with plasma obtained from FH subjects the platelet response to aggregating agents was significantly increased. Incubation of washed platelets from the FH patients with normal plasma, however, resulted in a significant decrease in platelet activity. Our data suggest that the increased platelet activation in FH patients is the result of a change in the platelets induced by abnormal plasma constituents.Thrombosis Research 05/1982; 26(2):101-9. DOI:10.1016/0049-3848(82)90019-6 · 2.45 Impact Factor