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Targeted deletion of murine coagulation factor XII gene-a model for contact phase activation in vivo

Hans-Ulrich Pauer1, Thomas Renné, Bernhard Hemmerlein

  • 1Department of Gynecology and Obstetrics, Medical School, University of Goettingen, Germany.

Thrombosis and Haemostasis
|September 8, 2004
PubMed

Insights

Factor XII (FXII) deficiency in mice did not impact hemostasis or pregnancy. These FXII knockout mice are valuable tools for studying FXII

Area of Science:

  • * Hematology and Coagulation Biology
  • * Genetics and Molecular Biology

Background:

  • * Factor XII (FXII), also known as Hageman Factor, plays a role in the intrinsic pathway of the coagulation cascade.
  • * Its precise in vivo biological functions, particularly in hemostasis and thrombosis, remain incompletely understood.
  • * Understanding FXII's role is crucial for developing targeted therapies for bleeding and clotting disorders.

Purpose of the Study:

  • * To investigate the in vivo biological role of Factor XII (FXII) by generating and analyzing FXII-deficient mice.
  • * To assess the impact of FXII deficiency on hemostasis, thrombosis, fibrinolysis, and reproductive outcomes.
  • * To establish a valuable animal model for further research into FXII's functions in health and disease.

Main Methods:

  • * Gene targeting approach used to generate homozygous FXII knockout (FXII(-/-)) mice on mixed and inbred genetic backgrounds.
  • * Analysis of plasma FXII activity and activated partial thromboplastin time (aPTT) in FXII(-/-) mice.
  • * Evaluation of coagulation factor levels, fetal loss, litter size, and gross/histological anatomy in FXII(-/-) mice compared to wild-type littermates.

Main Results:

  • * FXII(-/-) mice exhibited no detectable plasma FXII activity and a significantly prolonged aPTT.
  • * Levels of other key coagulation factors (XI, VIII, IX, X, VII, V, II, fibrinogen) were comparable between FXII(-/-) and wild-type mice.
  • * FXII deficiency did not lead to increased fetal loss, affect pregnancy outcomes, or alter gross/histological anatomy.

Conclusions:

  • * Murine FXII deficiency does not appear to cause thrombophilia or impaired fibrinolysis in vivo.
  • * FXII deficiency does not significantly affect overall hemostasis in mice.
  • * The generated FXII(-/-) mice serve as a critical resource for future studies elucidating the specific biological roles of FXII.

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