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PKCdelta regulates collagen-induced platelet aggregation through inhibition of VASP-mediated filopodia formation

Giordano Pula1, Kai Schuh, Keiko Nakayama

  • 1Department of Pharmacology, School of Medical Sciences, University of Bristol, United Kingdom.

Blood
|August 31, 2006
PubMed

Insights

Protein kinase Cdelta (PKCdelta) negatively regulates platelet aggregation by controlling filopodia formation. This regulation occurs via interaction with vasodilator-stimulated phosphoprotein (VASP), a key actin cytoskeleton organizer.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Hematology

Background:

  • Protein kinase Cdelta (PKCdelta) is known to inhibit collagen-induced platelet aggregation.
  • The precise molecular mechanisms behind this inhibitory role require elucidation.

Purpose of the Study:

  • To investigate the cellular and molecular mechanisms by which PKCdelta negatively regulates platelet aggregation.
  • To identify the key downstream effectors of PKCdelta in this process.

Main Methods:

  • Utilized PKCdelta knockout (PKCdelta-/-) and wild-type (WT) platelets.
  • Assessed integrin alpha(IIb)beta3 signaling, tyrosine phosphorylation of PLCgamma2, and dense granule secretion.
  • Analyzed filopodia generation and actin polymerization upon collagen adhesion.
  • Investigated the interaction between PKCdelta and vasodilator-stimulated phosphoprotein (VASP).

Main Results:

  • PKCdelta deficiency did not alter integrin alpha(IIb)beta3 signaling or early GPVI-dependent PLCgamma2 phosphorylation.
  • PKCdelta-/- platelets exhibited significantly enhanced filopodia generation upon collagen adhesion.
  • PKCdelta directly interacts with VASP, regulating its phosphorylation at Ser157.
  • VASP deficiency abrogated rottlerin-induced enhancement of filopodia, actin polymerization, and platelet aggregation.

Conclusions:

  • PKCdelta acts as a crucial negative regulator of platelet filopodia formation.
  • This regulation is mediated through a functional interaction with VASP, a key regulator of actin dynamics.
  • PKCdelta's control over VASP influences platelet aggregation by modulating filopodia generation and actin polymerization.

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