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Mouse Complete Stasis Model of Inferior Vena Cava Thrombosis
Published on: June 15, 2011
Characterization of a mouse model for thrombomodulin deficiency
H Weiler1, V Lindner, B Kerlin
1Blood Research Institute, Blood Center of Southeastern Wisconsin, Medical College of Wisconsin, Milwaukee, WI, USA.
Arteriosclerosis, Thrombosis, and Vascular Biology
|September 15, 2001
Summary
Thrombomodulin (TM) gene mutations increase thrombosis risk. TM(Pro/Pro) mice show heightened susceptibility to blood clots and sepsis, demonstrating TM
Area of Science:
- Biochemistry
- Genetics
- Immunology
Background:
- Mutations in thrombomodulin (TM), a thrombin regulator, are linked to thrombotic diseases.
- TM plays a crucial role in regulating coagulation and inflammation.
Purpose of the Study:
- To investigate the in vivo role of TM in thrombosis and endotoxin response.
- To characterize the TM(Pro/Pro) mouse model for thrombotic disease research.
Main Methods:
- Generation and characterization of TM(Pro/Pro) mice.
- Assessment of thrombosis using FeCl(3)-induced injury and carotid artery ligation models.
- Evaluation of endotoxin sensitivity and cytokine production.
Main Results:
- TM(Pro/Pro) mice exhibit a hypercoagulable state and increased susceptibility to thrombosis.
- Mutant mice showed accelerated platelet thrombus growth and precipitated thrombosis after vascular stasis.
- Increased mortality and altered cytokine profiles were observed in response to endotoxin.
Conclusions:
- TM is a critical regulator of both platelet- and coagulation-driven thrombosis in vivo.
- Genetic background significantly influences the penetrance of TM mutations.
- TM plays a role in modulating the inflammatory response to endotoxin.
