This study investigates the role of factor XIIIa (FXIIIa)-mediated fibrin γ-chain cross-linking in thrombus stability and the incidence of pulmonary embolism (PE). The research examines how the absence of γ-chain cross-linking affects thrombus resolution and embolization in a murine model.
Mice lacking fibrin γ-chain cross-linking exhibited increased rates of pulmonary embolism originating from inferior vena cava thrombi, indicating that γ-chain cross-linking by FXIIIa is crucial for thrombus stability and prevention of embolization.
The study utilized a genetically modified mouse model with a point mutation in the fibrinogen γ-chain (Fgg) gene, specifically altering the FXIIIa cross-linking site. This mutation prevents the cross-linking of fibrin γ-chains, allowing for the assessment of its role in thrombus stability and PE.
Thrombosis, Pulmonary embolism, Coagulation, Fibrin cross-linking, Hemostasis
Point mutation, Fibrinogen modification, Thrombosis model, Coagulation factor analysis, Genetic engineering
From model design to experimental results
Tailor-made solutions adapted to scientific questions
Comprehensive dataset package
Generated with biopharma partners and in-house
Scientific follow-up and advice along the project
Collaborative approach for problem solving and development of innovative models
Breeding facilities in US and Europe
Certified health status from professional breeders
