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The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
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Activated human platelets induce factor XIIa-mediated contact activation.

Jennie Bäck1, Javier Sanchez, Graciela Elgue

  • 1Departments of Oncology, Radiology, and Clinical Immunology, Division of Clinical Immunology, Rudbeck Laboratory C5, Uppsala University, SE-751 85 Uppsala, Sweden.

Biochemical and Biophysical Research Communications
|November 3, 2009
PubMed
Summary

Platelet activation triggers Factor XII (FXII)-mediated contact activation in human blood, contributing to clot formation. This process involves FXIIa-antithrombin complexes and highlights platelets

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Published on: May 23, 2025

Area of Science:

  • Hematology
  • Hemostasis and Thrombosis
  • Immunology

Background:

  • Platelets can activate Factor XII (FXII) in vitro under specific conditions.
  • The role of activated platelets in FXII activation within a physiological environment remains unclear.

Purpose of the Study:

  • To investigate if activated platelets induce FXII-mediated contact activation in human blood.
  • To determine the effect of this activation on clot formation.

Main Methods:

  • Human platelets were activated using thrombin receptor-activating peptide (TRAP) in platelet-rich plasma and whole blood.
  • Contact activation proteins (FXII, FXI, HMWK, PK) were detected on platelets via flow cytometry.
  • Enzymatic activity of FXIIa, FXIa, and kallikrein was measured using chromogenic assays.
  • FXIIa inhibition was assessed in non-anticoagulated blood.

Main Results:

  • Activated platelets generated FXIIa and FXIa, forming complexes with antithrombin (AT) and C1-inhibitor (C1INH).
  • This contact activation was independent of tissue factor or thrombin.
  • FXIIa-AT and FXIa-AT complexes were specifically formed in clotting whole blood.
  • Inhibition of FXIIa prolonged clotting time, confirming its role.

Conclusions:

  • Platelet activation initiates FXII-mediated contact activation on and near activated platelets.
  • This process generates FXIIa-AT and FXIa-AT complexes, contributing to thrombus formation.
  • Activated platelets serve as a site for intravascular contact activation, explaining FXII's importance in thrombus formation.