PI3 kinase-dependent stimulation of platelet migration by stromal cell-derived factor 1 (SDF-1)

Platelets have been regarded as static cells that do not move once they adhere to a matrix. The present study explored, whether platelets are able to migrate. In contrast to the current opinion, we found that platelets were mobile, able to migrate over a surface, and transmigrate through a transwell...

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Veröffentlicht in:Journal of molecular medicine (Berlin, Germany) Germany), 2010-12, Vol.88 (12), p.1277-1288
Hauptverfasser: Kraemer, Bjoern F., Borst, Oliver, Gehring, Eva-Maria, Schoenberger, Tanja, Urban, Benjamin, Ninci, Elena, Seizer, Peter, Schmidt, Christine, Bigalke, Boris, Koch, Miriam, Martinovic, Ivo, Daub, Karin, Merz, Tobias, Schwanitz, Laura, Stellos, Konstantinos, Fiesel, Fabienne, Schaller, Martin, Lang, Florian, Gawaz, Meinrad, Lindemann, Stephan
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Sprache:eng
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Zusammenfassung:Platelets have been regarded as static cells that do not move once they adhere to a matrix. The present study explored, whether platelets are able to migrate. In contrast to the current opinion, we found that platelets were mobile, able to migrate over a surface, and transmigrate through a transwell membrane and endothelium toward a source of stromal cell-derived factor 1 (SDF-1). Platelet migration was stimulated by SDF-1, which led to the downstream activation and phosphorylation of Wiskott–Aldrich syndrome protein. SDF-1 signaling and subsequent platelet migration could be inhibited by CXCR4-receptor blocker AMD3100, pertussis toxin, inhibition of phosphoinositol 3-kinase (PI3 kinase) with LY294002 or wortmannin, and disruption of actin polymerization with cytochalasin B. The potential of platelets to migrate in an SDF-1-mediated fashion may redefine the role of platelets in the pathophysiology of vascular inflammation, subsequent atherosclerotic degeneration, and vascular regeneration.
ISSN:0946-2716
1432-1440
DOI:10.1007/s00109-010-0680-8