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

Bjoern F. Kraemer, Oliver Borst, Eva Maria Gehring, Tanja Schoenberger, Benjamin Urban, Elena Ninci, Peter Seizer, Christine Schmidt, Boris Bigalke, Miriam Koch, Ivo Martinovic, Karin Daub, Tobias Merz, Laura Schwanitz, Konstantinos Stellos, Fabienne Fiesel, Martin Schaller, Florian Lang, Meinrad Gawaz, Stephan Lindemann

Research output: Contribution to journalArticlepeer-review

61 Scopus citations


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 cellderived 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.

Original languageEnglish (US)
Pages (from-to)1277-1288
Number of pages12
JournalJournal of Molecular Medicine
Issue number12
StatePublished - Dec 2010


  • Cell migration
  • Cell signaling
  • Inflammation
  • Platelets
  • SDF-1

ASJC Scopus subject areas

  • Molecular Medicine
  • Drug Discovery
  • Genetics(clinical)


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