Journal
CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
Volume 30, Issue 1, Pages 259-268Publisher
KARGER
DOI: 10.1159/000339062
Keywords
Platelets; Migration; SDF-1; WASP; Vinculin; SGK1
Categories
Funding
- Deutsche Forschungsgemeinschaft [KF0274, SFB-TR19]
- Fortune programme [1934-0-0, 1910-0-0]
Ask authors/readers for more resources
Recent observations pointed to the ability of platelets to migrate and thus to invade the inflamed vascular wall. Platelet migration could be stimulated by stromal cell-derived factor-1 (SDF-1), an effect dependent on phosphatidylinositide-3-kinase (PI3K) and paralleled by activation and phosphorylation of Wiskott-Aldrich syndrome protein (WASP). Migration is inhibited by vinculin, which is similarly regulated by phosphorylation. PI3K-sensitive kinases include the serum- and glucocorticoid-inducible kinase 1 (SGK1). The present study explored whether SGK1 modifies WASP and vinculin phosphorylation in murine platelets and participates in the regulation of platelet migration. Platelets were isolated from gene-targeted mice lacking SGK1 (sgk1(-/-)) and from their wild type littermates (sgk1(+/+)). Platelet migration stimulated with SDF-1 was significantly less pronounced in sgk1(-/-) platelets than in sgk1(+/+) platelets. Moreover, SDF-1 significantly induced WASP phosphorylation, an effect again reduced in platelets lacking SGK1. Phosphorylation of vinculin was significantly enhanced in sgk1(-/-) platelets and was significantly reduced following treatment of platelets with Ca2+ chelator BAPTA. Immunohistochemical analysis of in vivo experiments in intestinal vessels after vascular inflammation revealed that transmigration of platelets into inflamed vessel walls was significantly less pronounced in sgk1(-/-) than in sgk1(+/+) mice. In conclusion, SGK1 is a powerful regulator of platelet migration. Copyright (c) 2012 S. Karger AG, Basel
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available