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Activated human pla...
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Bäck, JennieUppsala universitet,Enheten för klinisk immunologi
(författare)
Activated human platelets induce factor XIIa-mediated contact activation
- Artikel/kapitelEngelska2010
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Elsevier BV,2010
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LIBRIS-ID:oai:DiVA.org:uu-124283
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https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-124283URI
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https://doi.org/10.1016/j.bbrc.2009.10.123DOI
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https://urn.kb.se/resolve?urn=urn:nbn:se:lnu:diva-2173URI
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Språk:engelska
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Sammanfattning på:engelska
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Ämneskategori:art swepub-publicationtype
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Earlier studies have shown that isolated platelets in buffer systems can promote activation of FXII or amplify contact activation, in the presence of a 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 thrombin. 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 on 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 on 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.
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Biuppslag (personer, institutioner, konferenser, titlar ...)
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Sanchez, JavierUppsala universitet,Enheten för klinisk immunologi(Swepub:uu)jasan991
(författare)
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Elgue, GracielaUppsala universitet,Enheten för klinisk immunologi(Swepub:uu)gracelgu
(författare)
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Ekdahl, Kristina NilssonLinnéuniversitetet,Uppsala universitet,Enheten för klinisk immunologi,Institutionen för naturvetenskap, NV(Swepub:lnu)nnikr
(författare)
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Nilsson, BoUppsala universitet,Enheten för klinisk immunologi(Swepub:uu)bonils
(författare)
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Uppsala universitetEnheten för klinisk immunologi
(creator_code:org_t)
Sammanhörande titlar
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Ingår i:Biochemical and Biophysical Research Communications - BBRC: Elsevier BV391:1, s. 11-170006-291X1090-2104
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