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Mer receptor tyrosine kinase signaling participates in platelet function

Cailin Chen1, Quan Li, Andrew L Darrow

  • 1Johnson & Johnson Pharmaceutical Research and Development, LLC, Spring House, PA 19477-0776, USA.

Arteriosclerosis, Thrombosis, and Vascular Biology
|May 8, 2004
PubMed
Abstract

Insights

Growth arrest-specific gene 6 product (Gas6) signaling regulates platelet function. Mer, a Gas6 receptor, is crucial for platelet aggregation and thrombosis in vivo, as demonstrated in mer-deficient mice.

Area of Science:

  • Hematology
  • Molecular Biology
  • Thrombosis Research

Background:

  • Growth arrest-specific gene 6 product (Gas6) deficiency leads to platelet dysfunction and reduced thrombosis susceptibility.
  • The specific Gas6 receptor(s) mediating these effects in platelets remain to be fully elucidated.

Purpose of the Study:

  • To identify and characterize the Gas6 receptor(s) involved in platelet function.
  • To investigate the role of the mer receptor in platelet aggregation and thrombosis.

Main Methods:

  • RT-PCR and Western blot analysis to determine mer, axl, and rse expression in platelets.
  • Generation of mer-deficient mice via gene targeting.
  • In vitro platelet aggregation assays using various agonists (collagen, U46619, PAR4 peptide, ADP).
  • In vivo thrombosis models: collagen/epinephrine-induced pulmonary thromboembolism and ferric chloride-induced thrombosis.

Main Results:

  • Mer was the predominant Gas6 receptor subtype expressed in mouse and human platelets; axl and rse were not detected.
  • Mer-deficient platelets showed reduced aggregation in response to collagen, U46619, and PAR4 peptide, but not ADP.
  • Mer-deficient mice exhibited protection from pulmonary thromboembolism and inhibited ferric chloride-induced thrombosis.
  • Coagulation, bleeding times, and peripheral blood cell counts were unaffected in mer-deficient mice.

Conclusions:

  • Mer is the primary Gas6 receptor in platelets, regulating platelet function in vitro.
  • Mer signaling is essential for platelet-dependent thrombosis in vivo.

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