[Amplification and inhibition of platelet function by serum lipoproteins].
Low-density lipoprotein (LDL) at a concentration of 100 micrograms/mL, which is near the dissociation constant (Kd) of LDL-binding, had a maximal stimulatory effect on agonist-induced platelet aggregation. Anti-LDL receptor monoclonal antibody (C-7), like native LDL, induces a transient increase in intracellular Ca2+ and a shape change of human platelets. On the other hand, high-density lipoprotein (HDL) inhibited platelet function. ApoE-rich HDL, as well as, apoE.DMPC potently inhibited platelet aggregation in a dose-dependent manner. ApoE.DMPC stimulated the release of cholesterol into the supernatant, suggesting that apoE plays a major role in the inhibitory effect of apoE-rich HDL in platelet function, presumably due to the release of cholesterol from the plasma membrane.
Higashihara
M
M
First Department of Internal Medicine, Faculty of Medicine, University of Tokyo.
D001057:Apolipoproteins E / Q000502:physiology*; D001792:Blood Platelets / Q000502:physiology*; D002118:Calcium / Q000097:blood; D002462:Cell Membrane / Q000378:metabolism; D002784:Cholesterol / Q000378:metabolism; D004134:Dimyristoylphosphatidylcholine / Q000494:pharmacology; D006801:Humans; D008075:Lipoproteins, HDL / Q000502:physiology*; D008077:Lipoproteins, LDL / Q000502:physiology*; D010974:Platelet Aggregation
D001057:Apolipoproteins E; D008075:Lipoproteins, HDL; D008077:Lipoproteins, LDL; D002784:Cholesterol; D002118:Calcium; D004134:Dimyristoylphosphatidylcholine