Published online before print January 13, 2006

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(Journal of Leukocyte Biology. 2006;79:499-507.)
© 2006 by Society for Leukocyte Biology

Platelet binding to monocytes increases the adhesive properties of monocytes by up-regulating the expression and functionality of ß₁ and ß₂ integrins

Paula A. da Costa Martins^*,1, Janine M. van Gils, Anita Mol, Peter L. Hordijk and Jaap J. Zwaginga^*,

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

¹ Correspondence: Sanquin Research (CLB), Dept. of Experimental Immunohematology (P112), Plesmanlaan 125, 1066 CX Amsterdam, The Netherlands. E-mail: p.martinsdacosta{at}sanquin.nl

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 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 ₄ß₁ and _Mß₂integrin, 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 ß₁ and ß₂integrins 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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