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Ferric Chloride-induced Thrombosis Mouse Model on Carotid Artery and Mesentery Vessel
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CD248 enhances tissue factor procoagulant function, promoting arterial and venous thrombosis in mouse models
Piyushkumar R Kapopara1, Nooshin S Safikhan1, Jenny L Huang1
1Centre for Blood Research, Life Sciences Institute, Faculty of Medicine, University of British Columbia, Vancouver, British Columbia, Canada.
Journal of Thrombosis and Haemostasis : JTH
|April 8, 2021
Summary
CD248 protein plays a role in blood clot formation by influencing the tissue factor pathway. Blocking CD248 may offer a new therapeutic strategy for thrombosis.
Area of Science:
- Biochemistry
- Hematology
- Molecular Biology
Background:
- CD248 is a pro-inflammatory glycoprotein found on vascular smooth muscle cells and monocytes.
- Its characteristics resemble those of tissue factor (TF), a key initiator of coagulation.
Purpose of the Study:
- To investigate the potential role of CD248 in thrombosis.
- To explore the functional interaction between CD248 and the TF-FVIIa-FX complex.
Main Methods:
- Utilized mouse models of vascular injury (ferric chloride-induced carotid artery occlusion and inferior vena cava stenosis).
- Assessed coagulation parameters including prothrombin time and activated partial thromboplastin time.
- Employed proximity ligation assays and conformation-specific antibodies to study TF-CD248 interactions.
Main Results:
- CD248 knockout mice exhibited delayed carotid artery occlusion and resistance to IVC stenosis-induced thrombosis.
- CD248 was found in close proximity to TF (<40 nm).
- CD248 enhanced TF-FVIIa-mediated factor X activation by inducing allosteric changes in the TF-FVIIa-FX complex.
Conclusions:
- CD248 is a novel protein partner within the TF-FVIIa-FX complex.
- CD248 modulates coagulation and represents a potential therapeutic target for thrombotic disorders.
