Platelet secretory products increase low density lipoprotein oxidation, enhance its uptake by macrophages, and reduce its fluidity.

Abstract

Oxidized low density lipoprotein (Ox-LDL) is considered to be involved in the atherogenic process. Factors influencing the formation of Ox-LDL are thus of importance. Oxidation of LDL in a cell-free system in the presence of copper ions was significantly increased (up to 60%) by the presence of platelet-conditioned medium, (PCM) obtained from collagen-activated platelets for the duration of the oxidation period. The effect was time- and dose-dependent and was related to hydrogen peroxide and superoxide production, since PCM-induced enhanced LDL oxidation was inhibited by catalase and by superoxide dismutase, but not by protease treatments. PCM also reduced the fluidity of oxidized LDL by 45%. Upon incubation with a J-774 macrophage-like cell line, PCM-treated Ox-LDL enhanced cellular cholesteryl ester synthesis by 47% and lipoprotein degradation by 41%. Thus platelet secretory products appeared to enhance LDL oxidation through the involvement of oxidative agents. The resulting Ox-LDL demonstrated increased atherogenic properties.