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

doi:10.1007/s00109-010-0680-8

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

Neuroscience

Research output: Contribution to journal › Article › peer-review

61 Scopus citations

Abstract

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 language	English (US)
Pages (from-to)	1277-1288
Number of pages	12
Journal	Journal of Molecular Medicine
Volume	88
Issue number	12
DOIs	https://doi.org/10.1007/s00109-010-0680-8
State	Published - Dec 2010

Keywords

Cell migration
Cell signaling
Inflammation
Platelets
SDF-1

ASJC Scopus subject areas

Molecular Medicine
Drug Discovery
Genetics(clinical)

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10.1007/s00109-010-0680-8

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Kraemer, B. F., Borst, O., Gehring, E. M., Schoenberger, T., Urban, B., Ninci, E., Seizer, P., Schmidt, C., Bigalke, B., Koch, M., Martinovic, I., Daub, K., Merz, T., Schwanitz, L., Stellos, K., Fiesel, F., Schaller, M., Lang, F., Gawaz, M., & Lindemann, S. (2010). PI3 kinase-dependent stimulation of platelet migration by stromal cell-derived factor 1 (SDF-1). Journal of Molecular Medicine, 88(12), 1277-1288. https://doi.org/10.1007/s00109-010-0680-8

Kraemer, BF, Borst, O, Gehring, EM, Schoenberger, T, Urban, B, Ninci, E, Seizer, P, Schmidt, C, Bigalke, B, Koch, M, Martinovic, I, Daub, K, Merz, T, Schwanitz, L, Stellos, K, Fiesel, F, Schaller, M, Lang, F, Gawaz, M & Lindemann, S 2010, 'PI3 kinase-dependent stimulation of platelet migration by stromal cell-derived factor 1 (SDF-1)', Journal of Molecular Medicine, vol. 88, no. 12, pp. 1277-1288. https://doi.org/10.1007/s00109-010-0680-8

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abstract = "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.",

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

note = "Funding Information: Acknowledgements We thank Jadwiga Kwiatkowska, Christina Neff, and Birgit Fehrenbacher for providing outstanding technical assistance and Uwe Renzland for the help in preparing and formatting the movies. This study was supported by the Deutsche Forschungsgemeinschaft (Li 849/3-1 to S.L., SFB-TR19 TP B8 to K.S., M.G., and S.L.), the fort{\"u}ne programme (1934-0-0 to O.B.) and the Karl-Kuhn-Stiftung (to S.L.).",

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AU - Kraemer, Bjoern F.

AU - Borst, Oliver

AU - Gehring, Eva Maria

AU - Schoenberger, Tanja

AU - Urban, Benjamin

AU - Ninci, Elena

AU - Seizer, Peter

AU - Schmidt, Christine

AU - Bigalke, Boris

AU - Koch, Miriam

AU - Martinovic, Ivo

AU - Daub, Karin

AU - Merz, Tobias

AU - Schwanitz, Laura

AU - Stellos, Konstantinos

AU - Fiesel, Fabienne

AU - Schaller, Martin

AU - Lang, Florian

AU - Gawaz, Meinrad

AU - Lindemann, Stephan

N1 - Funding Information: Acknowledgements We thank Jadwiga Kwiatkowska, Christina Neff, and Birgit Fehrenbacher for providing outstanding technical assistance and Uwe Renzland for the help in preparing and formatting the movies. This study was supported by the Deutsche Forschungsgemeinschaft (Li 849/3-1 to S.L., SFB-TR19 TP B8 to K.S., M.G., and S.L.), the fortüne programme (1934-0-0 to O.B.) and the Karl-Kuhn-Stiftung (to S.L.).

PY - 2010/12

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N2 - 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.

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ER -

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

Abstract

Keywords

ASJC Scopus subject areas

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