BACKGROUND: 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. METHODS AND RESULTS: 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. CONCLUSIONS: Cholesterol sulfate supports platelet adhesion and may be one of the factors determining the prothrombotic potential of atherosclerotic lesions.
BACKGROUND: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. METHODS AND RESULTS: 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. CONCLUSIONS:Cholesterol sulfate supports platelet adhesion and may be one of the factors determining the prothrombotic potential of atherosclerotic lesions.
Authors: Kye Hun Kim; Sook Hee Cho; Yi Rang Yim; Kyung Jin Lee; Ju Hyup Yum; Hyun Ju Yoon; Nam Sik Yoon; Young Joon Hong; Hyung Wook Park; Ju Han Kim; Youngkeun Ahn; Myung Ho Jeong; Jeong Gwan Cho; Jong Chun Park Journal: J Cardiovasc Ultrasound Date: 2013-06-26
Authors: Giuseppe Astarita; Jennifer H McKenzie; Bin Wang; Katrin Strassburg; Angela Doneanu; Jay Johnson; Andrew Baker; Thomas Hankemeier; James Murphy; Rob J Vreeken; James Langridge; Jing X Kang Journal: PLoS One Date: 2014-04-23 Impact factor: 3.240
Authors: Caroline H Johnson; Antonio F Santidrian; Sarah E LeBoeuf; Michael E Kurczy; Nicholas J W Rattray; Zahra Rattray; Benedikt Warth; Melissa Ritland; Linh T Hoang; Celine Loriot; Jason Higa; James E Hansen; Brunhilde H Felding; Gary Siuzdak Journal: Cancer Metab Date: 2017-10-31