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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2009;29:620.)
© 2009 American Heart Association, Inc.

Editorials

Statin Islands and PPAR Ligands in Platelets

Richard P. Phipps; Neil Blumberg

From the University of Rochester School of Medicine and Dentistry, Departments of Environmental Medicine and Pathology & Laboratory Medicine, NY.

Correspondence to Dr Richard P. Phipps, University of Rochester School of Medicine and Dentistry, Department of Environmental Medicine, Box 850, 601 Elmwood Ave, Rochester, NY 14642. E-mail Richard_Phipps@urmc.rochester.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Platelets are formed from megakaryocytes, where they are released into the blood stream via proplatelet extensions into the blood vessel lumen.¹ Being the most numerous "white blood cell" and despite lacking a nucleus, they are highly complex cells containing a surface connected canalicular and tubular system, mitochondria, granules, and bioactive mediators. Platelets are well-known for their seminal role in hemostasis and thrombosis.² Aside from these physiological functions, new roles for platelets are being identified in unwanted thrombosis that occurs in diabetes and cancer.

See accompanying article on page 706

Platelets have been thought of as a kind of "cellular island" owing to their traditional role as mere hemostatic plugs. However, recent studies show that platelets are much more than simple cellular elements involved in sealing wounds. They are now recognized as highly interactive cells that influence both bone marrow–derived and nonbone marrow–derived cells.² They accomplish this by their ability to release and synthesize a host of mediators that influence other cell types. For example, platelets produce a variety of important cytokines such as TGFβ and lipid mediators such as prostaglandins that stimulate many types of cells. Platelets also express and release CD40 ligand (CD154), which can quickly activate CD40-bearing cells such as B lymphocytes, neutrophils, macrophages, dendritic cells, and platelets themselves.^3–5 These CD40-bearing cells then become stimulated to produce antibody in the case of B cells⁶ or become activated to increase their ability to present antigen⁷ (dendritic cells) or kill invading microorganisms (neutrophils).⁸ Thus, the "new view" of platelets is . . . [Full Text of this Article]

Related Article:

Antiplatelet Actions of Statins and Fibrates Are Mediated by PPARs

Ferhana Y. Ali, Paul C.J. Armstrong, Al-Rehan A. Dhanji, Arthur T. Tucker, Mark J. Paul-Clark, Jane A. Mitchell, and Timothy D. Warner
Arterioscler Thromb Vasc Biol 2009 29: 706-711. [Abstract] [Full Text] [PDF]