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C-reactive protein inhibit complement-mediated platelet activation suggesting a protective role in atherogenesis
Linköping University, Department of Medicine and Care, Pharmacology. Linköping University, Faculty of Health Sciences.
Linköping University, Department of Molecular and Clinical Medicine, Rheumatology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Centre for Medicine, Department of Rheumatology in Östergötland.
Linköping University, Department of Molecular and Clinical Medicine, Rheumatology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Centre for Medicine, Department of Rheumatology in Östergötland.ORCID iD: 0000-0002-0153-9249
Linköping University, Department of Molecular and Clinical Medicine, Rheumatology. Linköping University, Faculty of Health Sciences.ORCID iD: 0000-0002-6916-5490
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2006 (English)In: Atherosclerosis Supplements, ISSN 1567-5688, E-ISSN 1878-5050, Vol. 7, no 3, 284-284 p.Article in journal, Meeting abstract (Other academic) Published
Abstract [en]

  Objective: C-reactive protein (CRP) represents a powerful predictor of coro- nary artery disease. However, its physiological role is not fully understood. The binding of CRP to its ligand phosphorylcholine (PC) activates the com- plement system via the classical pathway, although limited to the initial stages, i.e. no membrane attack complex is formed. The aim of this study was to chaxacterize CRP-induced complement activation on PC-coated surfaces, and to investigate the regulatory effects of PC-bound crp on complement induced platelet activation.

Methods: PC conjugated to keyhole limpet hemocyanin was immobilized to cross-linked fibrinogen on silica particles. Ellipsometry and polyclonal anti- bodies were used to quantify deposition of serum proteins, complement factors and CRP on the surfaces. Washed platelets as well as serum were prepared according to standard protocols. CRP concentrations were measured with a high sensitivity assay. Lumi-aggregometry was used to evaluate the effects of PC-coated particles and CRP on complement-induced platelet aggregation and secretion.

Results: Serum (5%) induced platelet aggregation and secretion through complement-dependent mechanisms. PC-coated particles antagonized the complement-mediated platelet activation but only if CRP was present. Inter- estingly, we found that a minor elevation of CRR below 5 rag/1 was sufficient to inhibit platelet activation.

Conclusions: We suggest that CRP bound to PC-expressing ligands, e.g. bacteria or modified low-density lipoproteins in an atherosclerotic lesion, modulate complement activation and thereby prevent a harmful platelet activation.

Place, publisher, year, edition, pages
Clare, Ireland: Elsevier, 2006. Vol. 7, no 3, 284-284 p.
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Natural Sciences
Identifiers
URN: urn:nbn:se:liu:diva-39504DOI: 10.1016/S1567-5688(06)81153-0ISI: 000239093901563Local ID: 49061OAI: oai:DiVA.org:liu-39504DiVA: diva2:260353
Conference
14th Meeting of the International-Society-of-Atherosclerosis, Rome, Italy, June 18-22 2006
Available from: 2009-10-10 Created: 2009-10-10 Last updated: 2017-12-13Bibliographically approved

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Skoglund, CarolineSjöwall, ChristofferSkogh, ThomasWetterö, JonasTengvall, PenttiBengtsson, Torbjörn

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Skoglund, CarolineSjöwall, ChristofferSkogh, ThomasWetterö, JonasTengvall, PenttiBengtsson, Torbjörn
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PharmacologyFaculty of Health SciencesRheumatologyDepartment of Rheumatology in ÖstergötlandApplied PhysicsThe Institute of Technology
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Atherosclerosis Supplements
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