Cholesterol-enriched human platelets released significantly more arachidonic acid (18.1% vs 14.6%, P<0.001) and converted more to thromboxane B2 than cholesterol-depleted platelets in vitro.
Does cholesterol enrichment increase arachidonic acid metabolism and thromboxane B2 production in human platelets in vitro?
In vitro cholesterol enrichment of human platelets significantly increases arachidonic acid release and thromboxane B2 production, providing a mechanistic link between cholesterol levels and platelet reactivity.
Absolute Event Rate: 18.1% vs 14.6%
p-value: p=<0.001
We altered platelet cholesterol by incubating the cells with either "cholesterol-rich" or "cholesterol-poor" liposomes. These platelets were then used to study the influence of cholesterol content on the metabolism of arachidonic acid, a fatty acid that serves as the critical precursor in the platelet for formation of the potent aggregating agent thromboxane A2. After addition of the aggregating agent thrombin, cholesterol-enriched platelets released 18.1 +/- 0.6 per cent (mean +/- 1 S.E.M.) 14Carachidonic acid from prelabeled platelet phospholipids. This value was higher (P less than 0.001) than that for cholesterol-depleted platelets (14.6 +/- 1.0 per cent). Conversion of released arachidonic acid to platelet thromboxane B2 (the stable end product of thromboxane A2) was also higher in cholesterol-rich platelets (22.6 +/- 3.9 per cent) than in cholesterol-depleted platelets (13.8 +/- 2.7 per cent). These studies show that changes in the cholesterol content of human platelets in vitro have a significant effect on platelt metabolism of arachidonic acid. N Engl J Med 302:6-10, 1980).
Stuart et al. (Thu,) conducted a other in Platelet metabolism. Cholesterol-rich liposomes vs. Cholesterol-poor liposomes was evaluated on Release of [14C]arachidonic acid from prelabeled platelet phospholipids after addition of thrombin (p=<0.001). Cholesterol-enriched human platelets released significantly more arachidonic acid (18.1% vs 14.6%, P<0.001) and converted more to thromboxane B2 than cholesterol-depleted platelets in vitro.