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A novel transgenic mouse model of hyperfibrinogenemia
A A Gulledge1, F Rezaee, J H Verheijen
1University of North Carolina at Chapel Hill, 27599-7525, USA.
Thrombosis and Haemostasis
|August 28, 2001
Summary
Elevated fibrinogen (hyperfibrinogenemia) did not cause disease in a new mouse model. Further studies will explore its role in disease initiation and progression.
Area of Science:
- Biochemistry
- Genetics
- Pathophysiology
Background:
- Hyperfibrinogenemia is a known risk predictor for cardiovascular disease.
- The etiological role of elevated fibrinogen in disease pathogenesis remains unclear.
Purpose of the Study:
- To investigate whether elevated fibrinogen directly causes disease.
- To develop a mouse model for studying hyperfibrinogenemia.
Main Methods:
- Generated transgenic mice overexpressing all three fibrinogen genes.
- Liver-specific transgene expression was confirmed via Northern blot.
- Assessed fibrinogen function and mouse health through immunologic, clotting assays, and histological examination.
Main Results:
- Successfully created a hyperfibrinogenemia mouse model with 1.7-fold elevated fibrinogen.
- Transgene expression was liver-specific, with message levels 2- to 3-fold enhanced.
- Transgenic mice showed no increased mortality, morbidity, or organ abnormalities compared to controls.
Conclusions:
- Overexpression of all three fibrinogen genes is required for hyperfibrinogenemia.
- Elevated fibrinogen alone did not induce disease in this mouse model.
- Future research will involve breeding these mice with disease models to assess fibrinogen's role in disease initiation and progression.