Intracellular mechanisms in the activation of human platelets by low-density lipoproteins.
Low-density lipoproteins (LDL) have been shown to cause aggregation of human blood platelets at concentrations above 2 g of protein/l. The secretion of the contents of platelet dense granules was detected, but not that of the lysosomes. LDL gave rise to a mobilization of [3H]arachidonic acid from phospholipids and the appearance of products of the cyclo-oxygenase pathway after only 10 s. LDL-promoted aggregation was inhibited by both aspirin and indomethacin. There was an increase in 3H-labelled diacylglycerols and the phosphorylation of 47 kDa proteins. LDL therefore shares at least some of the mechanisms of stimulus/response coupling with those of other agonists.
D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000097:blood; D001792:Blood Platelets / Q000187:drug effects* / Q000378:metabolism; D001798:Blood Proteins / Q000378:metabolism; D004075:Diglycerides / Q000097:blood; D006801:Humans; D007424:Intracellular Fluid / Q000378:metabolism; D008077:Lipoproteins, LDL / Q000494:pharmacology*; D010766:Phosphorylation; D010974:Platelet Aggregation / Q000187:drug effects
C011439:1,2-diacylglycerol; D001095:Arachidonic Acids; D001798:Blood Proteins; D004075:Diglycerides; D008077:Lipoproteins, LDL; D016718:Arachidonic Acid