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Updated: May 11, 2026
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A Mouse Model of in Utero Transplantation
Published on: January 28, 2011
Complete antithrombin deficiency in mice results in embryonic lethality
K Ishiguro1, T Kojima, K Kadomatsu
1First Department of Internal Medicine, Nagoya University School of Medicine, Nagoya, Japan.
The Journal of Clinical Investigation
|October 6, 2000
Summary
Antithrombin (ATIII) is crucial for embryonic development. Gene disruption in mice led to embryonic death by 16.5 days due to severe bleeding, highlighting ATIII
Area of Science:
- Biochemistry
- Developmental Biology
- Hematology
Background:
- Antithrombin (ATIII) is a key plasma protease inhibitor regulating blood coagulation.
- Maintaining blood fluidity is essential for physiological processes, including embryogenesis.
Purpose of the Study:
- To investigate the role of antithrombin in embryonic development using a gene disruption model.
- To elucidate the consequences of antithrombin deficiency during mouse embryogenesis.
Main Methods:
- Targeted gene disruption in mice to create antithrombin-deficient (ATIII(-/-)) embryos.
- Genotyping and histological examination of embryos at various gestational ages (gd).
- Analysis of fibrin(ogen) deposition and hemorrhage in affected embryos.
Main Results:
- Antithrombin-deficient embryos exhibited normal Mendelian distribution until 14.5 gd.
- Significant embryonic lethality observed from 15.5 gd onwards, with 100% mortality by 16.5 gd.
- Extensive subcutaneous hemorrhage and fibrin(ogen) deposition in the myocardium and liver of ATIII(-/-) embryos.
Conclusions:
- Antithrombin is essential for embryonic survival, indicating a critical role in development.
- Antithrombin deficiency leads to dysregulated blood coagulation, particularly affecting the myocardium and liver.
- Consumptive coagulopathy and/or liver dysfunction likely contribute to the observed pathology in antithrombin-deficient embryos.
