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piggyBac Transposon System Modification of Primary Human T Cells
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Recombinant pig TFPI efficiently regulates human tissue factor pathways.

K F Eddy Lee1, Evelyn J Salvaris, Jean-Christian Roussel

  • 1Immunology Research Centre, St. Vincent's Health, Melbourne, Vic., Australia.

Xenotransplantation
|July 10, 2008
PubMed
Summary
This summary is machine-generated.

Pig tissue factor pathway inhibitor (TFPI) does not cause incompatibility in xenograft rejection. This study found pig TFPI functions equivalently to human TFPI, ruling it out as a cause of thrombosis in pig-to-primate transplants.

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Area of Science:

  • Xenotransplantation research
  • Coagulation and thrombosis
  • Molecular incompatibility in organ transplantation

Background:

  • Pig-to-primate organ xenografts frequently suffer microvascular thrombosis.
  • This thrombosis is partly attributed to molecular incompatibilities in coagulation regulation.

Purpose of the Study:

  • To investigate potential functional incompatibility of pig tissue factor pathway inhibitor (TFPI) with human coagulation factors.
  • To determine if pig TFPI impedes human factor Xa binding or regulation of human tissue factor-initiated coagulation.

Main Methods:

  • Cloned TFPIalpha cDNA from pig aortic endothelial cells.
  • Expressed GPI-linked pig and human TFPIalpha in transfected primate cells.
  • Assayed binding of human factor Xa and inhibition of the human factor VIIa/tissue factor complex.

Main Results:

  • Pig TFPIalpha shares high sequence identity (79-90%) with human TFPIalpha, particularly in functional domains.
  • Expressed pig TFPI demonstrated equivalent anticoagulant activity to human TFPI in binding and inhibition assays.
  • No functional incompatibility was observed between recombinant pig TFPI and the human tissue factor pathway.

Conclusions:

  • Pig TFPI is functionally compatible with the human coagulation system.
  • TFPI incompatibility is not the cause of thromboregulatory failure in pig-to-primate xenograft rejection.
  • Other molecular factors likely contribute to aberrant tissue factor activity and thrombosis in xenografts.