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dc.contributor.authorSchroder, WA
dc.contributor.authorLe, TT
dc.contributor.authorGardner, J
dc.contributor.authorAndrews, RK
dc.contributor.authorGardiner, EE
dc.contributor.authorCallaway, L
dc.contributor.authorSuhrbier, A
dc.date.accessioned2020-02-26T01:26:42Z
dc.date.available2020-02-26T01:26:42Z
dc.date.issued2019
dc.identifier.issn0953-7104
dc.identifier.doi10.1080/09537104.2018.1535702
dc.identifier.urihttp://hdl.handle.net/10072/391915
dc.description.abstractSerpinB2, also known as plasminogen activation inhibitor type 2 (PAI-2), is classically viewed as an inhibitor of fibrinolysis. However, we show herein a distinct, hitherto unrecognized role for SerpinB2 in hemostasis. Mice deficient in SerpinB2 expression and mice with an active site mutation in SerpinB2, both showed significant reductions in tail bleeding times. This hemostatic phenotype was associated with platelets, with SerpinB2 and SerpinB2-urokinase complexes clearly present in platelet fractions, and immunohistochemistry of blood clots suggesting SerpinB2 is associated with platelet aggregates. Thromboelastography illustrated faster onset of clot formation in blood from SerpinB2 deficient mice, whereas clotting of platelet-free plasma was unaffected. The results appear consistent with the low circulating SerpinB2 levels and hypercoagulation seen during pre-eclampsia; however, SerpinB2 was not detected in human platelets.
dc.description.peerreviewedYes
dc.languageEnglish
dc.language.isoeng
dc.publisherRoutledge: Taylor & Francis Group
dc.relation.ispartofpagefrom658
dc.relation.ispartofpageto663
dc.relation.ispartofissue5
dc.relation.ispartofjournalPlatelets
dc.relation.ispartofvolume30
dc.subject.fieldofresearchClinical Sciences
dc.subject.fieldofresearchMedical Physiology
dc.subject.fieldofresearchcode1103
dc.subject.fieldofresearchcode1116
dc.subject.keywordsBleeding times
dc.subject.keywordsPAI-2
dc.subject.keywordsSerpinB2
dc.subject.keywordsplasminogen activation inhibitor type 2
dc.subject.keywordsplatelet
dc.titleSerpinB2 deficiency in mice reduces bleeding times via dysregulated platelet activation
dc.typeJournal article
dc.type.descriptionC1 - Articles
dcterms.bibliographicCitationSchroder, WA; Le, TT; Gardner, J; Andrews, RK; Gardiner, EE; Callaway, L; Suhrbier, A, SerpinB2 deficiency in mice reduces bleeding times via dysregulated platelet activation, Platelets, 2019, 30 (5), pp. 658-663
dcterms.licensehttp://creativecommons.org/licenses/by-nc-nd/4.0/
dc.date.updated2020-02-26T01:23:45Z
dc.description.versionVersion of Record (VoR)
gro.rights.copyright© 2018 The Author(s). Published with license by Taylor & Francis Group, LLC. This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License (http://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited, and is not altered, transformed, or built upon in any way.
gro.hasfulltextFull Text
gro.griffith.authorSchroder, Wayne


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