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(Circulation Research. 2000;87:81.)
© 2000 American Heart Association, Inc.

Editorial

Smooth Muscle Cells

Another Source of Tissue Factor–Containing Microparticles in Atherothrombosis?

Alain Tedgui, Ziad Mallat

From the Institut National de la Santé et de la Recherche Médicale, INSERM U541 and Institut Fédératif de Recherche "Circulation Paris-7," Hôpital Lariboisière, Paris, France.

Correspondence to Alain Tedgui, PhD, INSERM U541, 41, Bd de la Chapelle, 75475 Paris Cedex 10, France. E-mail tedgui@infobiogen.fr

Key Words: muscle, smooth • thromboplastin • atherosclerosis • thrombosis • microparticles

	Introduction

 
Severe clinical manifestations of atherosclerosis, including sudden death, myocardial infarction, and stroke, mainly result from atherosclerotic plaque rupture/erosion that triggers thrombus formation, leading to occlusion of the vessel lumen.¹ The occluding thrombus is mixed in nature and contains significant quantities of fibrin in addition to platelets,² suggesting an important role for the coagulation cascade in plaque thrombus formation. Tissue factor (TF), a 47-kDa transmembrane glycoprotein, is known to be the key element in the initiation of the extrinsic pathway of the coagulation cascade and appears to be a critical determinant of atherosclerotic plaque thrombogenicity.^{3 4 5} Yet, the origin of active TF within the plaque has not been well established.

Analysis of coronary atherectomy specimens from patients with unstable angina showed a strong correlation between TF content and areas of macrophages and smooth muscle cells, suggesting cell-mediated thrombogenicity.⁶ However, the acellular lipid-rich core of an atherosclerotic plaque exhibits the most intense TF staining, and functional studies have shown that it represents the most thrombogenic part of the plaque.⁴ This suggests that plaque thrombogenicity is directly related to its extracellular TF content and that extracellular TF is responsible for a great majority of active TF in the plaque. We have recently shown that the enhanced activity of extracellular TF is directly related to the presence, in the lipid core, of TF-bearing–shed membrane microparticles that are rich in phosphatidylserine (PS).⁵ The microparticles could be identified by use of capture antibodies against specific surface antigens and appeared to originate mainly from macrophages and lymphocytes.⁵ These . . . [Full Text of this Article]

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