Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-7372
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dc.contributor.authorKiouptsi, Klytaimnistra-
dc.contributor.authorGrill, Alexandra-
dc.contributor.authorMann, Amrit-
dc.contributor.authorDöhrmann, Mareike-
dc.contributor.authorLillich, Maren-
dc.contributor.authorJäckel, Sven-
dc.contributor.authorMalinarich, Frano-
dc.contributor.authorFormes, Henning-
dc.contributor.authorManukyan, Davit-
dc.contributor.authorSubramaniam, Saravanan-
dc.contributor.authorKhandagale, Avinash-
dc.contributor.authorKarwot, Cornelia-
dc.contributor.authorThal, Serge-
dc.contributor.authorBosmann, Markus-
dc.contributor.authorScharrer, Inge-
dc.contributor.authorJurk, Kerstin-
dc.contributor.authorReinhardt, Christoph-
dc.date.accessioned2022-07-12T07:53:23Z-
dc.date.available2022-07-12T07:53:23Z-
dc.date.issued2017
dc.identifier.urihttps://openscience.ub.uni-mainz.de/handle/20.500.12030/7386-
dc.description.abstractVon Willebrand factor (VWF) is the carrier protein of the anti-haemophilic Factor VIII (FVIII) in plasma. It has been reported that the infusion of FVIII concentrate in haemophilia A patients results in lowered VWF plasma levels. However, the impact of F8-deficiency on VWF plasma levels in F8-/y mice is unresolved. In order to avoid confounding variables, we back-crossed F8-deficient mice onto a pure C57BL/6J background and analysed VWF plasma concentrations relative to C57BL/6J WT (F8+/y) littermate controls. F8-/y mice showed strongly elevated VWF plasma concentrations and signs of hepatic inflammation, as indicated by increased TNF-α, CD45, and TLR4 transcripts and by elevated macrophage counts in the liver. Furthermore, immunohistochemistry showed that expression of VWF antigen was significantly enhanced in the hepatic endothelium of F8-/y mice, most likely resulting from increased macrophage recruitment. There were no signs of liver damage, as judged by glutamate-pyruvate-transaminase (GPT) and glutamate-oxalacetate-transaminase (GOT) in the plasma and no signs of systemic inflammation, as white blood cell subsets were unchanged. As expected, impaired haemostasis was reflected by joint bleeding, prolonged in vitro clotting time and decreased platelet-dependent thrombin generation. Our results point towards a novel role of FVIII, synthesized by the liver endothelium, in the control of hepatic low-grade inflammation and VWF plasma levels.en_GB
dc.description.sponsorshipDFG, Open Access-Publizieren Universität Mainz / Universitätsmedizinde
dc.language.isoengde
dc.rightsCC0*
dc.rights.urihttps://creativecommons.org/publicdomain/zero/1.0/*
dc.subject.ddc610 Medizinde_DE
dc.subject.ddc610 Medical sciencesen_GB
dc.titleMice deficient in the anti-haemophilic coagulation factor VIII show increased von Willebrand factor plasma levelsen_GB
dc.typeZeitschriftenaufsatzde
dc.identifier.doihttp://doi.org/10.25358/openscience-7372-
jgu.type.dinitypearticleen_GB
jgu.type.versionPublished versionde
jgu.type.resourceTextde
jgu.organisation.departmentFB 04 Medizinde
jgu.organisation.number2700-
jgu.organisation.nameJohannes Gutenberg-Universität Mainz-
jgu.rights.accessrightsopenAccess-
jgu.journal.titlePLOS ONEde
jgu.journal.volume12de
jgu.journal.issue8de
jgu.pages.alternativee0183590de
jgu.publisher.year2017-
jgu.publisher.namePLOSde
jgu.publisher.placeSan Francisco, California, USde
jgu.publisher.urihttp://dx.doi.org/10.1371/journal.pone.0183590de
jgu.publisher.issn1932-6203de
jgu.organisation.placeMainz-
jgu.subject.ddccode610de
opus.date.modified2018-04-04T10:45:15Z
opus.subject.dfgcode00-000
opus.organisation.stringFB 04: Medizin: Klinik für Anästhesiologiede_DE
opus.organisation.stringFB 04: Medizin: III. Medizinische Klinik und Poliklinikde_DE
opus.organisation.stringFB 04: Medizin: Centrum für Thrombose und Hämostase (CTH)de_DE
opus.identifier.opusid57991
opus.institute.number0418
opus.institute.number0427
opus.institute.number0463
opus.metadataonlyfalse
opus.type.contenttypeKeinede_DE
opus.type.contenttypeNoneen_EN
opus.affiliatedThal, Serge
opus.affiliatedScharrer, Inge
opus.affiliatedReinhardt, Christoph
jgu.publisher.doi10.1371/journal.pone.0183590de
jgu.organisation.rorhttps://ror.org/023b0x485
Appears in collections:DFG-OA-Publizieren (2012 - 2017)

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