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Altered phospholipid metabolism in thrombin-stimulated human platelets.

Extensive research during the past few years has indicated that dramatic alterations in phospholipid metabolism and composition represent early and important biochemical events in the response of human platelets to thrombin stimulation. The individual enzyme-catalyzed steps which provide for the release of free arachidonic acid for thromboxane A2 formation via the initial degradation of phosphatidylcholine and phosphatidylinositol have been studied. Their importance in this regard is influenced by the molecular species composition of the corresponding phospholipid precursors. A role for stimulated phosphatidylinositol 4,5-bisphosphate degradation in the phosphatidylinositol response and inositol triphosphate release associated with calcium mobilization has also been proposed. The 1,2-diacylglycerol released by the action of phospholipase C on phosphatidylinositol and its 4,5-bisphosphate derivative has been implicated as an activator of protein phosphorylation; the derived phosphatidic acid has been proposed as a mediator for promoting an intracellular flux of calcium associated with platelet responses.