Platelet signaling–A primer

Authors

  • Robert Goggs BVSc, DACVECC, MRCVS,

    Corresponding author
    • From the School of Physiology and Pharmacology, Faculty of Medical and Veterinary Sciences, University of Bristol, UK
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  • Alastair W. Poole MA, VetMB, PhD


  • Robert Goggs is supported by a Wellcome Trust research training fellowship. The British Heart Foundation, the Wellcome Trust, the Medical Research Council, and the Biotechnology and Biological Sciences Research Council support work in Prof. Alastair Poole's laboratory.

  • The authors declare no conflict of interest.

Address correspondence and reprint requests to

Mr. Robert Goggs, School of Physiology and Pharmacology, University of Bristol, Medical Sciences Building, University Walk, Bristol, BS8 1TD, United Kingdom.

Email: rob.goggs@bristol.ac.uk

Abstract

Objective

To review the receptors and signal transduction pathways involved in platelet plug formation and to highlight links between platelets, leukocytes, endothelium, and the coagulation system.

Data Sources

Original studies, review articles, and book chapters in the human and veterinary medical fields.

Data Synthesis

Platelets express numerous surface receptors. Critical among these are glycoprotein VI, the glycoprotein Ib-IX-V complex, integrin αIIbβ3, and the G-protein-coupled receptors for thrombin, ADP, and thromboxane. Activation of these receptors leads to various important functional events, in particular activation of the principal adhesion receptor αIIbβ3. Integrin activation allows binding of ligands such as fibrinogen, mediating platelet-platelet interaction in the process of aggregation. Signals activated by these receptors also couple to 3 other important functional events, secretion of granule contents, change in cell shape through cytoskeletal rearrangement, and procoagulant membrane expression. These processes generate a stable thrombus to limit blood loss and promote restoration of endothelial integrity.

Conclusions

Improvements in our understanding of how platelets operate through their signaling networks are critical for diagnosis of unusual primary hemostatic disorders and for rational antithrombotic drug design.

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