Journal
DIABETES & VASCULAR DISEASE RESEARCH
Volume 9, Issue 3, Pages 216-225Publisher
SAGE PUBLICATIONS LTD
DOI: 10.1177/1479164111432788
Keywords
Complement C3; inflammation; fibrin; fibrinolysis; thrombosis
Funding
- Medical Research Council DTA
- British Heart Foundation Clinical PhD studentship [FS/03/056]
- Swiss National Science Foundation
- Novartis Foundation
- German ADUMED foundation
- Special Trustees of the Leeds Teaching Hospitals NHS Trust (UK)
- EU [LSHM-CT-2004-005268]
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Background and method: Increased plasma clot density and prolonged lysis times are associated with cardiovascular disease. In this study, we employed a functional proteomics approach to identify novel clot components which may influence clot phenotypes. Results: Analysis of perfused, solubilised plasma clots identified inflammatory proteins, including complement C3, as novel clot components. Analysis of paired plasma and serum samples confirmed concentration-dependent incorporation of C3 into clots. Surface plasmon resonance indicated high-affinity binding interactions between C3 and fibrinogen and fibrin. Turbidimetric clotting and lysis assays indicated C3 impaired fibrinolysis in a concentration-dependent manner, both in vitro and ex vivo. Conclusion: These data indicate functional interactions between complement C3 and fibrin leading to prolonged fibrinolysis. These interactions are physiologically relevant in the context of protection following injury and suggest a mechanistic link between increased plasma C3 concentration and acute cardiovascular thrombotic events.
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