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(Circulation. 2002;106:1433.)
© 2002 American Heart Association, Inc.

Platelets, Endothelial Cells, Inflammatory Chemokines, and Restenosis

Complex Signaling in the Vascular Play Book

Andrew S. Weyrich, PhD; Stephen M. Prescott, MD; Guy A. Zimmerman, MD

From the Department of Internal Medicine (A.S.W., S.M.P., G.A.Z.), The Huntsman Cancer Institute (S.M.P.), and The Program in Human Molecular Biology and Genetics (A.S.W., G.A.Z.), The University of Utah, Salt Lake City.

Correspondence to Guy Zimmerman, Program in Human Molecular Biology and Genetics, Eccles Institute of Human Genetics, 15 N 2030 East, Bldg. 533, Rm. 4220, University of Utah, Salt Lake City, UT 84112. E-mail guy.zimmerman@hmbg.utah.edu

Key Words: Editorials • endothelium • platelets • leukocytes • inflammation

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

Adhesive and signaling interactions between endothelial cells and leukocytes are key mechanisms that mediate both targeting of the blood cells to specific sites and information transfer that results in change in their phenotypes and function.¹ These events are beneficial in defense against microbes and wound surveillance and repair; however, in dysregulated inflammatory conditions such as atherosclerosis and its complications, including acute coronary syndromes and restenosis after interventional procedures, accumulation and activation of leukocytes can injure the host. The cell–cell interactions and signaling mechanisms are complex in the game of inflammation, and there are a number of players. In addition to endothelial cells and leukocytes, platelets contribute to leukocyte accumulation and to changes in their behavior in both physiological and pathological conditions,^2,3,4 emphasizing the intimate relationship between the thrombotic and inflammatory systems.

See p 1523

One mechanism involves direct adhesion of activated platelets to monocytes, neutrophils, or other leukocyte subclasses and binding of chemokines or lipid signaling molecules that are released from the platelets or displayed in a juxtacrine fashion on their surfaces (see below), to receptors on the leukocyte plasma membrane.^3,5 In this issue of Circulation, Schober and co-workers⁶ report a different play in the inflammatory repertoire: platelets interacting with inflamed endothelial cells donate the CC chemokine regulated upon activation normal T cell expressed presumed secreted (RANTES) to the endothelial surface, where it acts as a cell-associated signal for adhesion of monocytes. A number of the observations were made with cultured endothelial monolayers, incubated under conditions of stasis or . . . [Full Text of this Article]

Related Article:

Deposition of Platelet RANTES Triggering Monocyte Recruitment Requires P-Selectin and Is Involved in Neointima Formation After Arterial Injury

Andreas Schober, David Manka, Philipp von Hundelshausen, Yuqing Huo, Peter Hanrath, Ian J. Sarembock, Klaus Ley, and Christian Weber
Circulation 2002 106: 1523-1529. [Abstract] [Full Text]

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