Thrombin-induced platelet activation is enhanced by very low and low density lipoproteins but decreased by high density lipoprotein in vitro.
In vitro, VLDL and LDL enhance platelet activation while HDL decreases it, providing a mechanistic link between lipoprotein profiles and thrombotic risk.
Thrombin-induced platelet activation is enhanced by very low and low density lipoproteins but decreased by high density lipoprotein. Plasma lipoproteins maximally affect platelet aggregation and 14C-serotonin release in a gel-filtered platelet preparation within 10 min of incubation at 37 degrees C. This effect is saturable and physiologic concentrations of lipoproteins are required in order to attain this saturation. When no aggregating agent is added to the incubation medium, the lipoproteins alone did not alter platelet aggregation. However, 14C-serotonin release is increased by very-low- and low-density lipoproteins alone more than by high density lipoprotein. On removal of the lipoproteins after incubation with the platelets, and subsequent testing of platelet function, minimal influence of these lipoproteins on the platelet function remains. Arachidonic acid causes similar results to thrombin when added to the platelet suspension after incubation with the lipoprotein. Our results further emphasize the 'opposing effects' of very low and low density lipoproteins as compared to high density lipoproteins on platelets and/or platelet-thrombin interaction.
Jacob G. Brook (2009) studied this question. Plasma lipoproteins (VLDL, LDL, HDL) was evaluated on Platelet aggregation and 14C-serotonin release. Thrombin-induced platelet activation is enhanced by very low and low density lipoproteins but decreased by high density lipoprotein in vitro.