Cholesterol sulfate : A new adhesive molecule for platelets

Cholesterol 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. In this study, we investigated the interaction of platelets with cholesterol sulfate. Platelets adhered in...

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Bibliographic Details
Published in:	Circulation (New York, N.Y.) N.Y.), 2001-04, Vol.103 (16), p.2032-2034
Main Authors:	MERTEN, Michael, JING FEI DONG, LOPEZ, Jose A, THIAGARAJAN, Perumal
Format:	Article
Language:	eng
Subjects:	Antibodies - pharmacology Atherosclerosis (general aspects, experimental research) Biological and medical sciences Blood and lymphatic vessels Blood Platelets - drug effects Blood Platelets - metabolism Cardiology. Vascular system Cell Adhesion - drug effects Cell Separation Cholesterol - analogs & derivatives Cholesterol - chemistry Cholesterol - pharmacology Cholesterol Esters - chemistry Cholesterol Esters - metabolism Cholesterol Esters - pharmacology Diffusion Chambers, Culture Dose-Response Relationship, Drug Humans Medical sciences Platelet Activation Platelet Adhesiveness - drug effects Platelet Membrane Glycoproteins - antagonists & inhibitors Rheology Surface Properties Thrombospondins - antagonists & inhibitors von Willebrand Factor - antagonists & inhibitors
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Summary:	Cholesterol 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. In 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. Cholesterol sulfate supports platelet adhesion and may be one of the factors determining the prothrombotic potential of atherosclerotic lesions.
ISSN:	0009-7322 1524-4539