Roles of SLP-76, phosphoinositide 3-kinase, and gelsolin in the platelet shape changes initiated by the collagen receptor GPVI/FcRγ-chain complex

H. Falet, K. L. Barkalow, V. I. Pivniouk, M. J. Barnes, R. S. Gena, J. H. Hartwig

Research output: Contribution to journalArticlepeer-review

50 Scopus citations

Abstract

How platelet shape change initiated by a collagen-related peptide (CRP) specific for the GPVI/FcRγ-chain complex (GPVI/FcRγ-chain) is coupled to SLP-76, phosphoinositide (PI) 3-kinase, and gelsolin is reported. As shown by video microscopy, platelets rapidly round and grow dynamic filopodial projections that rotate around the periphery of the cell after they contact a CRP-coated surface. Lamellae subsequently spread between the projections. All the actin-driven shape changes require SLP-76 expression. SLP-76 is essential for the Ca++ mobilization induced by CRP, whereas PI 3-kinase only modulates it. The extension of lamellae requires net actin assembly and an exposure of actin filament barbed ends downstream of PI 3-kinase. Gelsolin expression is also required for the extension of lamellae, but not for the formation of filopodia. Altogether, the data describe the role of SLP-76 in the platelet activation initiated by GPVI/FcRγ-chain and the roles of PI 3-kinase and gelsolin in lamellae spreading. (C) 2000 by The American Society of Hematology.

Original languageEnglish (US)
Pages (from-to)3786-3792
Number of pages7
JournalBlood
Volume96
Issue number12
DOIs
StatePublished - Dec 1 2000
Externally publishedYes

ASJC Scopus subject areas

  • Biochemistry
  • Immunology
  • Hematology
  • Cell Biology

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