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.
Intracellular mechanisms in the activation of human platelets by low-density lipoproteins
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H E Andrews, J W Aitken, D G Hassall, V O Skinner, K R Bruckdorfer; Intracellular mechanisms in the activation of human platelets by low-density lipoproteins. Biochem J 1 March 1987; 242 (2): 559–564. doi: https://doi.org/10.1042/bj2420559
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