(Circulation. 2001;103:2032.)
© 2001 American Heart Association, Inc.
Brief Rapid Communications |
From the Department of Internal Medicine, University of Texas Health Science Center (M.M., P.T.), and the Department of Medicine, Baylor College of Medicine (J.F.D., J.A.L.), Houston, Tex.
Correspondence to Perumal Thiagarajan, MD, University of Texas at Houston Medical School, 6431 Fannin, MSB 5.284, Houston, TX 77030. E-mail Perumal.Thiagarajan{at}uth.tmc.edu
BackgroundCholesterol 3-sulfate is present on a variety of cells and in human LDL, and it has been found in atherosclerotic lesions of human aorta. Its precise biological role has not yet been described.
Methods and ResultsIn this study, we investigated the interaction of platelets with cholesterol sulfate. Platelets adhered in a concentration-dependent and saturable manner to cholesterol sulfate but did not adhere to cholesterol, cholesterol acetate, estrone sulfate, or dehydroepiandrosterone sulfate, suggesting that the specificity of this interaction is determined not only by the cholesterol moiety but also by the sulfate group. This adhesion did not increase after platelet activation, and it was not cation-dependent. Soluble cholesterol sulfate inhibited adhesion in a concentration-dependent manner. However, antibodies against glycoprotein Ib, glycoprotein IIb/IIIa, CD36, P-selectin, von Willebrand factor, or thrombospondin had no significant effect on platelet adhesion to cholesterol sulfate. Perfusion of whole blood in a parallel-plate flow chamber resulted in the rapid and progressive adhesion of platelets to cholesterol sulfate but not to cholesterol acetate or estrone sulfate.
ConclusionsCholesterol sulfate supports platelet adhesion and may be one of the factors determining the prothrombotic potential of atherosclerotic lesions.
Key Words: atherosclerosis thrombosis cell adhesion molecules
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