ArticleJournal of immunology (Baltimore, Md. : 1950)2010
Complement component C3 binds to activated normal platelets without preceding proteolytic activation and promotes binding to complement receptor 1.
Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 120 citations in OpenAlex.
- The hidden battlefield: platelet function in the wake of severe trauma.Frontiers in immunology · 2026Review
- Cardiovascular risk factors associated with BMI and metabolic health phenotypes based on measures of coagulation factors.International journal of obesity (2005) · 2025Article
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- Modeling antithymocyte globulin-induced microvasculopathy using human iPSC-derived vascularized liver organoids.Cell reports. Medicine · 2025Article
- Native C3 is activated without proteolytic cleavage by transformation to C3(HFrontiers in immunology · 2025Article
- Thromboinflammation vs. immunothrombosis: strategies for overcoming anticoagulant resistance in COVID-19 and other hyperinflammatory diseases. Is ROTEM helpful or not?Frontiers in immunology · 2025Review
- Platelets in infection: intrinsic roles and functional outcomes.Frontiers in immunology · 2025Review
- Activation of platelets and the complement system in mice withAmerican journal of physiology. Lung cellular and molecular physiology · 2024Article
- Immunity and Coagulation in COVID-19.International journal of molecular sciences · 2024Review
- The Concept of Thromboinflammation.Hamostaseologie · 2024Review
- Storage of Transfusion Platelet Concentrates Is Associated with Complement Activation and Reduced Ability of Platelets to Respond to Protease-Activated Receptor-1 and Thromboxane A2 Receptor.International journal of molecular sciences · 2024Article
- Unraveling the Intricate Web: Complement Activation Shapes the Pathogenesis of Sepsis-Induced Coagulopathy.Journal of innate immunity · 2024Review
- The Role of the Complement System in the Pathogenesis of Infectious Forms of Hemolytic Uremic Syndrome.Biomolecules · 2023Review
- Protein therapeutics and their lessons: Expect the unexpected when inhibiting the multi-protein cascade of the complement system.Immunological reviews · 2023Review
- Fc galactosylation of anti-platelet human IgG1 alloantibodies enhances complement activation on platelets.Haematologica · 2022Article
- Coagulation and complement: Key innate defense participants in a seamless web.Frontiers in immunology · 2022Review
- Complement C3b contributes toFrontiers in immunology · 2022Article
- Shiga Toxin 2a Binds to Complement Components C3b and C5 and Upregulates Their Gene Expression in Human Cell Lines.Toxins · 2020Article
- Complement deposition, C4d, on platelets is associated with vascular events in systemic lupus erythematosus.Rheumatology (Oxford, England) · 2020Article
- The optimal incubation time for in vitro hemocompatibility testing: Assessment using polymer reference materials under pulsatile flow with physiological wall shear stress conditions.Journal of biomedical materials research. Part B, Applied biomaterials · 2019Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 3 countries.
Funding
Abstract
It has been reported that complement is activated on the surface of activated platelets, despite the presence of multiple regulators of complement activation. To reinvestigate the mechanisms by which activated platelets bind to complement components, the presence of complement proteins on the surfaces of nonactivated and thrombin receptor-activating peptide-activated platelets was analyzed by flow cytometry and Western blot analyses. C1q, C4, C3, and C9 were found to bind to thrombin receptor-activating peptide-activated platelets in lepirudin-anticoagulated platelet-rich plasma (PRP) and whole blood. However, inhibiting complement activation at the C1q or C3 level did not block the binding of C3 to activated platelets. Diluting PRP and chelating divalent cations also had no effect, further indicating that the deposition of complement components was independent of complement activation. Furthermore, washed, activated platelets bound added C1q and C3 to the same extent as platelets in PRP. The use of mAbs against different forms of C3 demonstrated that the bound C3 consisted of C3(H(2)O). Furthermore, exogenously added soluble complement receptor 1 was shown to bind to this form of platelet-bound C3. These observations indicate that there is no complement activation on the surface of platelets under physiological conditions. This situation is in direct contrast to a number of pathological conditions in which regulators of complement activation are lacking and thrombocytopenia and thrombotic disease are the ultimate result. However, the generation of C3(H(2)O) represents nonproteolytic activation of C3 and after factor I cleavage may act as a ligand for receptor binding.
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