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

Content Provider	Springer Nature Link
Author	Kraemer, Bjoern F. Borst, Oliver Gehring, Eva Maria Schoenberger, Tanja Urban, Benjamin Ninci, Elena Seizer, Peter Schmidt, Christine Bigalke, Boris Koch, Miriam Martivic, Ivo Daub, Karin Merz, Tobias Schwanitz, Laura Stellos, Konstantis Fiesel, Fabienne Schaller, Martin Lang, Florian Gawaz, Meinrad Lindemann, Stephan
Copyright Year	2010
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 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.
Starting Page	1277
Ending Page	1288
Page Count	12
File Format	PDF
ISSN	09462716
Journal	Journal of Molecular Medicine
Volume Number	88
Issue Number	12
e-ISSN	14321440
Language	English
Publisher	Springer-Verlag
Publisher Date	2010-09-18
Publisher Place	Berlin/Heidelberg
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Platelets SDF-1 Cell migration Cell signaling Inflammation Internal Medicine Human Genetics Molecular Medicine
Content Type	Text
Resource Type	Article
Subject	Drug Discovery Molecular Medicine Genetics (clinical)

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

VEGFR1/CXCR4-positive progenitor cells modulate local inflammation and augment tissue perfusion by a SDF-1-dependent mechanism

RAP1-GTPase signaling and platelet function

Stromal cell-derived factor 1- (sdf)-induced human t cell chemotaxis becomes phosphoinositide 3-kinase.

Stromal cell-derived factor 1- (SDF)-induced human T cell chemotaxis becomes phosphoinositide 3-kinase

Umbilical Cord Blood-Derived Stromal Cells Regulate Megakaryocytic Proliferation and Migration Through SDF-1/PECAM-1 Pathway

B cell antigen receptor engagement inhibits stromal cell–derived factor (sdf)-1 chemotaxis and promotes protein kinase c (pkc)-induced internalization of cxcr4 (1999).

Ocular neovascularization

Regulation of arterial blood pressure by Akt1-dependent vascular relaxation

Transendothelial Migration of Megakaryocytes in Response to Stromal Cell-derived Factor 1 (SDF-1) Enhances Platelet Formation

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

Similar Documents

VEGFR1/CXCR4-positive progenitor cells modulate local inflammation and augment tissue perfusion by a SDF-1-dependent mechanism

RAP1-GTPase signaling and platelet function

Stromal cell-derived factor 1- (sdf)-induced human t cell chemotaxis becomes phosphoinositide 3-kinase.

Stromal cell-derived factor 1- (SDF)-induced human T cell chemotaxis becomes phosphoinositide 3-kinase

Umbilical Cord Blood-Derived Stromal Cells Regulate Megakaryocytic Proliferation and Migration Through SDF-1/PECAM-1 Pathway

B cell antigen receptor engagement inhibits stromal cell–derived factor (sdf)-1 chemotaxis and promotes protein kinase c (pkc)-induced internalization of cxcr4 (1999).

Ocular neovascularization

Regulation of arterial blood pressure by Akt1-dependent vascular relaxation

Transendothelial Migration of Megakaryocytes in Response to Stromal Cell-derived Factor 1 (SDF-1) Enhances Platelet Formation

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