Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-7417
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dc.contributor.authorKiouptsi, Klytaimnistra-
dc.contributor.authorGambaryan, Stepan-
dc.contributor.authorWalter, Elena-
dc.contributor.authorWalter, Ulrich-
dc.contributor.authorJurk, Kerstin-
dc.contributor.authorReinhardt, Christoph-
dc.date.accessioned2022-07-14T08:24:34Z-
dc.date.available2022-07-14T08:24:34Z-
dc.date.issued2017
dc.identifier.urihttps://openscience.ub.uni-mainz.de/handle/20.500.12030/7431-
dc.description.abstractUnder ischemic conditions, tissues are exposed to hypoxia. Although human physiology, to a certain extent, can adapt to hypoxic conditions, the impact of low oxygen levels on platelet function is unresolved. Therefore, we explored how reduction of atmospheric oxygen levels to 1% might affect agonist-induced aggregation and static adhesion of isolated human platelets. We uncovered that isolated, washed human platelets exposed to hypoxic conditions show reduced thrombin receptor-activating peptide-6 (TRAP-6) and convulxin-induced aggregation. Of note, this hypoxia-triggered effect was not observed in platelet-rich plasma. Independent of the agonist used (TRAP-6, ADP), activation of the platelet fibrinogen receptor integrin αIIbβ3 (GPIIbIIIa, CD41/CD61) was strongly reduced at 1% and 8% oxygen. The difference in agonist-induced integrin αIIbβ3 activation was apparent within 5 minutes of stimulation. Following hypoxia, re-oxygenation resulted in the recovery of integrin αIIbβ3 activation. Importantly, platelet secretion was not impaired by hypoxia. Static adhesion experiments revealed decreased platelet deposition to fibrinogen coatings, but not to collagen or vitronectin coatings, indicating that specifically the function of the integrin subunit αIIb is impaired by exposure of platelets to reduced oxygen levels. Our results reveal an unexpected effect of oxygen deprivation on platelet aggregation mediated by the fibrinogen receptor integrin αIIbβ3.en_GB
dc.description.sponsorshipDFG, Open Access-Publizieren Universität Mainz / Universitätsmedizinde
dc.language.isoengde
dc.rightsCC BY*
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/*
dc.subject.ddc610 Medizinde_DE
dc.subject.ddc610 Medical sciencesen_GB
dc.titleHypoxia impairs agonist-induced integrin αIIbβ3 activation and platelet aggregationen_GB
dc.typeZeitschriftenaufsatzde
dc.identifier.doihttp://doi.org/10.25358/openscience-7417-
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.titleScientific reportsde
jgu.journal.volume7de
jgu.pages.alternativeArt. 7621de
jgu.publisher.year2017-
jgu.publisher.nameMacmillan Publishers Limited, part of Springer Naturede
jgu.publisher.placeLondonde
jgu.publisher.urihttp://dx.doi.org/10.1038/s41598-017-07988-xde
jgu.publisher.issn2045-2322de
jgu.organisation.placeMainz-
jgu.subject.ddccode610de
opus.date.modified2019-01-22T10:33:59Z
opus.subject.dfgcode00-000
opus.organisation.stringFB 04: Medizin: Centrum für Thrombose und Hämostase (CTH)de_DE
opus.identifier.opusid57990
opus.institute.number0463
opus.metadataonlyfalse
opus.type.contenttypeKeinede_DE
opus.type.contenttypeNoneen_EN
opus.affiliatedWalter, Ulrich
opus.affiliatedReinhardt, Christoph
jgu.publisher.doi10.1038/s41598-017-07988-xde
jgu.organisation.rorhttps://ror.org/023b0x485-
Appears in collections:DFG-OA-Publizieren (2012 - 2017)

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