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Related Experiment Video

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Extracellular Vesicle Tissue Factor Activity Assay
03:53

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Published on: December 29, 2023

Lipid-bound factor Xa regulates tissue factor activity.

James Hathcock1, Elena Rusinova, Heikki Vaananen

  • 1Mt. Sinai School of Medicine, Box #1269, Annenberg 24-92, One Gustave Levy Place, New York, New York 10029, USA. James.Hathcock@mssm.edu

Biochemistry
|May 2, 2007
PubMed
Summary

Product inhibition of blood coagulation factor X activation by tissue factor (TF) and factor VIIa (VIIa) can be overcome. Removing activated factor X (fXa) from the reaction enhances TF-VIIa activity, suggesting new models for coagulation initiation.

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Published on: September 9, 2012

Area of Science:

  • Biochemistry
  • Hematology
  • Molecular Biology

Background:

  • Blood coagulation initiation involves the activation of coagulation factor X (fX) by the tissue factor (TF) and coagulation factor VIIa (VIIa) complex on a phospholipid surface.
  • The product, activated factor X (fXa), transiently binds to the TF-VIIa complex, leading to probabilistic inhibition of subsequent fX activations.

Purpose of the Study:

  • To investigate the inhibitory role of the reaction product, fXa, in the TF-VIIa-catalyzed activation of fX.
  • To determine if enhancing fX activation can be achieved by manipulating fXa levels or its binding to the reaction site.

Main Methods:

  • Utilized benzamidine and soybean trypsin inhibitor-conjugated Sepharose beads to sequester fXa and remove it from the reaction.
  • Employed resonance energy transfer to measure the dissociation constants of fX and fXa for phospholipid vesicles.
  • Assessed the relationship between fXa binding to phospholipid surfaces and the rates of fX activation under various experimental conditions.

Main Results:

  • Sequestration of fXa using Sepharose beads significantly enhanced fX activation by the TF-VIIa complex.
  • Dissociation constants for fX and fXa binding to 100 nm phospholipid vesicles were determined to be in the range of 30-60 nM.
  • The rate of fX activation was found to be inversely dependent on the amount of fXa bound to the TF-phospholipid surface.

Conclusions:

  • Activated factor X (fXa) acts as an inhibitor in the initiation of blood coagulation.
  • Removal of fXa from the reaction zone, through flow, sequestration, or binding to distant lipid surfaces, enhances TF-VIIa activity.
  • Existing models of coagulation initiation require re-evaluation to incorporate product inhibition by fXa and its binding dynamics to the enzyme and phospholipid surface.