ArticleTH open : companion journal to thrombosis and haemostasis2018
Complement Component C3 Binds to the A3 Domain of von Willebrand Factor.
Article in TH open : companion journal to thrombosis and haemostasis, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Structure and multiple functions of von Willebrand factor.Haematologica · 2026Review
- The Immunology of Transfusion Medicine: Past, Present, and Future.Methods in molecular biology (Clifton, N.J.) · 2026Review
- Complement is activated in patients with acute chest syndrome caused by sickle cell disease and represents a therapeutic target.Science translational medicine · 2025Article
- Novel functions for von Willebrand factor.Blood · 2024Review
- Complement inhibition can decrease the haemostatic response in a microvascular bleeding model at multiple levels.Frontiers in immunology · 2023Article
- MASP-2 and MASP-3 inhibitors block complement activation, inflammation, and microvascular stasis in a murine model of vaso-occlusion in sickle cell disease.Translational research : the journal of laboratory and clinical medicine · 2022Article
- COVID-19 microthrombosis: unusually large VWF multimers are a platform for activation of the alternative complement pathway under cytokine storm.International journal of hematology · 2022Review
- Complement lectin pathway components MBL and MASP-1 promote haemostasis upon vessel injury in a microvascular bleeding model.Frontiers in immunology · 2022Article
- Comparative Analysis of Serum Proteins Between Hepatitis B Virus Genotypes B and C Infection by DIA-Based Quantitative Proteomics.Infection and drug resistance · 2021Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
von Willebrand factor (VWF) is a multimeric protein composed of monomeric subunits (~280 kD) linked by disulfide bonds. During hemostasis and thrombosis, ultralarge (UL) VWF (ULVWF) multimers initiate platelet adhesion. In vitro, human C3 binds to ULVWF multimeric strings secreted by and anchored to human endothelial cell to promote the assembly and activation of C3 convertase (C3bBb) and C5 convertase (C3bBbC3b) of the alternative complement pathway (AP). The purified and soluble C3 avidly binds to recombinant human VWF A1A2A3, as well as the recombinant isolated human VWF A3 domain. Notably, the binding of soluble human ULVWF multimers to purified human C3 was blocked by addition of a monovalent Fab fragment antibody to the VWF A3 domain. We conclude that the A3 domain in VWF/ULVWF contains a docking site for C3. In contrast, purified human C4, an essential component of the classical and lectin complement pathways, binds to soluble, isolated A1, but not to ULVWF strings secreted by and anchored to endothelial cells. Our findings should facilitate the design of new therapeutic agents to suppress the initiation of the AP on ULVWF multimeric strings during thrombotic and inflammatory disorders.
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