ArticlePloS one2010
Contribution of chondroitin sulfate A to the binding of complement proteins to activated platelets.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 46 citations in OpenAlex.
- Redox Regulation of Complement Pathway Activation in Aging and Related Diseases.Antioxidants (Basel, Switzerland) · 2025Review
- Impact of smoking on the complement system: a narrative review.Frontiers in immunology · 2025Review
- 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
- Analysis of normal levels of free glycosaminoglycans in urine and plasma in adults.The Journal of biological chemistry · 2022Article
- Complement C3b contributes toFrontiers in immunology · 2022Article
- Coagulation and complement: Key innate defense participants in a seamless web.Frontiers in immunology · 2022Review
- Interactions of adenoviruses with platelets and coagulation and the vaccine-induced immune thrombotic thrombocytopenia syndrome.Haematologica · 2021Review
- Predicting the In Vivo Performance of Cardiovascular Biomaterials: Current Approaches In Vitro Evaluation of Blood-Biomaterial Interactions.International journal of molecular sciences · 2021Review
- SARS-CoV-2: Pathogenic Mechanisms and Host Immune Response.Advances in experimental medicine and biology · 2021Article
- Complement in Hemolysis- and Thrombosis- Related Diseases.Frontiers in immunology · 2020Review
- Platelets and Complement Cross-Talk in Early Atherogenesis.Frontiers in cardiovascular medicine · 2019Review
- Evaluation of a Novel Immunoassay for Quantification of C1q for Clinical Diagnostic Use.Frontiers in immunology · 2019Article
- The Human Platelet as an Innate Immune Cell: Interactions Between Activated Platelets and the Complement System.Frontiers in immunology · 2019Review
- The non-haemostatic role of platelets in systemic lupus erythematosus.Nature reviews. Rheumatology · 2018Review
- Factor H C-Terminal Domains Are Critical for Regulation of Platelet/Granulocyte Aggregate Formation.Frontiers in immunology · 2017Article
- Properdin: a tightly regulated critical inflammatory modulator.Immunological reviews · 2016Review
- Complement inhibition in biomaterial- and biosurface-induced thromboinflammation.Seminars in immunology · 2016Review
- Properdin-Mediated C5a Production Enhances Stable Binding of Platelets to Granulocytes in Human Whole Blood.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Interactions between coagulation and complement--their role in inflammation.Seminars in immunopathology · 2012Review
- Article
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundExposure of chondroitin sulfate A (CS-A) on the surface of activated platelets is well established. The aim of the present study was to investigate to what extent CS-A contributes to the binding of the complement recognition molecule C1q and the complement regulators C1 inhibitor (C1INH), C4b-binding protein (C4BP), and factor H to platelets. PRINCIPAL
findingsHuman blood serum was passed over Sepharose conjugated with CS-A, and CS-A-specific binding proteins were identified by Western blotting and mass spectrometric analysis. C1q was shown to be the main protein that specifically bound to CS-A, but C4BP and factor H were also shown to interact. Binding of C1INH was dependent of the presence of C1q and then not bound to CS-A from C1q-depleted serum. The specific interactions observed of these proteins with CS-A were subsequently confirmed by surface plasmon resonance analysis using purified proteins. Importantly, C1q, C4BP, and factor H were also shown to bind to activated platelets and this interaction was inhibited by a CS-A-specific monoclonal antibody, thereby linking the binding of C1q, C4BP, and factor H to exposure of CS-A on activated platelets. CS-A-bound C1q was also shown to amplify the binding of model immune complexes to both microtiter plate-bound CS-A and to activated platelets.
conclusionsThis study supports the concept that CS-A contributes to the binding of C1q, C4BP, and factor H to platelets, thereby adding CS-A to the previously reported binding sites for these proteins on the platelet surface. CS-A-bound C1q also seems to amplify the binding of immune complexes to activated platelets, suggesting a role for this molecule in immune complex diseases.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.