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Activated platelets induce FXII-mediated contact activation
Linnaeus University, Faculty of Science and Engineering, School of Natural Sciences.ORCID iD: 0000-0001-7888-1571
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2010 (English)In: Biochemical and Biophysical Research Communications - BBRC, ISSN 0006-291X, E-ISSN 1090-2104, Vol. 391, no 1, p. 11-17Article in journal (Refereed) Published
Abstract [en]

Earlier studies have shown that isolated platelets in buffer systems can promote activation of FXII or amplify contact activation. in the presence of it negatively charge Substance or material Still proof is lacking that FXII is activated by platelets in a more physiological environment In this study we investigate if activated platelets can induce FXII-mediated contact activation and whether this activation affects clot formation in human blood.

Human platelets were activated with a thrombin receptor-activating peptide, SFLLRN-amide, in platelet-rich plasma or in whole blood. FXIIa and FXIa in complex with preferentially antithrombin (AT) and to some extent C1-inhibitor (C1INH) were generated in response to TRAP stimulation. This contact activation was independent of surface-mediated contact activation, tissue factor pathway or thiombin. In clotting whole blood FXIIa-AT and FXIa-AT complexes were specifically formed. demonstrating that AT is a potent inhibitor of FXIIa and FXIa generated by platelet activation Contact activation proteins were analyzed by flow cytometry and FXII, FXI, high-molecular weight kininogen, and prekallikrein were detected oil activated platelets Using chromogenic assays, enzymatic activity of platelet-associated FXIIa, FXIa, and kallikrein were demonstrated Inhibition of FXIIa in non-anticoagulated blood also prolonged the clotting time.

We conclude that platelet activation triggers FXII-mediated contact activation oil the Surface and in the vicinity of activated platelets This leads specifically to generation of FXIIa-AT and FXIa-AT complexes, and contributes to clot formation Activated platelets may thereby constitute an intravascular locus for contact activation, which may explain the recently reported importance of FXII in thrombus formation (C) 2009 Published by Elsevier Inc.

Place, publisher, year, edition, pages
2010. Vol. 391, no 1, p. 11-17
Keywords [en]
Antithrombin; Clot formation; Contact activation; Factor XII; Platelets
National Category
Immunology in the medical area
Research subject
Biomedical Sciences, Immunology
Identifiers
URN: urn:nbn:se:lnu:diva-2173DOI: 10.1016/j.bbrc.2009.10.123OAI: oai:DiVA.org:lnu-2173DiVA, id: diva2:309223
Available from: 2010-04-06 Created: 2010-04-06 Last updated: 2018-01-12Bibliographically approved

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Nilsson Ekdahl, Kristina

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