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Blood, 1 December 2000, Vol. 96, No. 12, pp. 3823-3826
HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY
Endogenous biosynthesis of thromboxane and prostacyclin in 2 distinct murine models of atherosclerosis
Domenico Praticò,
Tillmann Cyrus,
Hongwei Li, and
Garret A. FitzGerald
From the Center for Experimental Therapeutics,
University of Pennsylvania, School of Medicine, Philadelphia, PA.
Thromboxane A2 is a potent vasoconstrictor and platelet
agonist; prostacyclin is a potent platelet inhibitor and vasodilator. Altered biosynthesis of these eicosanoids is a feature of human hypercholesterolemia and atherosclerosis. This study examined whether
in 2 murine models of atherosclerosis their levels are increased and
correlated with the evolution of the disease. Urinary 2,3-dinor
thromboxane B2 and 2,3-dinor-6-keto prostaglandin
F1 , metabolites of thromboxane and prostacyclin,
respectively, were assayed in apoliprotein E
(apoE)-deficient mice on chow and low-density lipoprotein receptor
(LDLR)-deficient mice on chow and a Western-type diet. Atherosclerosis
lesion area was measured by en face method. Both
eicosanoids increased in apoE-deficient mice on chow and in
LDLR-deficient mice on a high-fat diet, but not in LDLR-deficient mice
on chow by the end of the study. Aspirin suppressed ex vivo platelet
aggregation, serum thromboxane B2, and 2,3-dinor
thromboxane B2, and significantly reduced the excretion of
2,3-dinor-6-keto prostaglandin F1 in these animals. This
study demonstrates that thromboxane as well as prostacyclin
biosynthesis is increased in 2 murine models of atherogenesis and is
secondary to increased in vivo platelet activation. Assessment of their
generation in these models may afford the basis for future studies on
the functional role of these eicosanoids in the evolution and
progression of atherosclerosis.
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