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Published online before print January 13, 2006
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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0605318

Received for publication June 15, 2005.
Revised November 18, 2005.
Accepted for publication November 21, 2005.

Article

Platelet binding to monocytes increases the adhesive properties of monocytes by up-regulating the expression and functionality of {beta}1 and {beta}2 integrins

Paula A. da Costa Martins *, Janine M. van Gils {dagger}, Anita Mol {dagger}, Peter L. Hordijk {dagger}, and Jaap J. Zwaginga *{ddagger}

Departments of *Experimental Immunohematology and {dagger}Molecular Cell Biology, Sanquin Research at CLB and Landsteiner Laboratory, Academic Medical Center, Amsterdam, The Netherlands; and {ddagger}Department of Immunohematology and Blood Transfusion, Leiden University Medical Center, The Netherlands


  Abstract

Human monocytes adhere to activated platelets, resulting in the formation of platelet-monocyte complexes (PMC). Complex formation depends on the interaction between platelet-displayed P-selectin and the specific ligand for P-selectin on leukocytes, P-selectin glycoprotein ligand-1 (PSGL-1). We have recently shown that monocytes within a PMC have increased adhesive capacity to the activated endothelium. To better understand the effect of platelet binding on the capacity of monocytes to adhere to activated endothelium, the P-selectin-PSGL-1 interaction-induced changes in integrin functionality were studied. The binding of platelets to monocytes via P-selectin-PSGL-1 interactions was shown to increase expression and activity of {alpha}4{beta}1 and {alpha}M{beta}2 integrin, with a concomitant decrease in L-selectin expression. Furthermore, the binding of platelets to monocytes resulted in increased monocyte adhesion to intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and fibronectin. Platelet binding was also responsible for an increase in monocyte transendothelial migration. Similar effects were observed after engagement of PSGL-1 with specific antibodies or with P-selectin immunoglobulin protein. Our data suggest that platelets, by binding via P-selectin to PSGL-1 on monocytes, induce up-regulation and activation of {beta}1 and {beta}2 integrins and increased adhesion of monocytes to activated endothelium. Hence, monocytes within PMC are in a higher state of activation and may have, therefore, an increased atherogenic capacity.

Key Words: endothelial cells • platelet-monocyte complexes • cell surface adhesion molecules • cell activation




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