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dc.contributor.authorErica M. Sparkenbaughen_US
dc.contributor.authorPichika Chantrathammacharten_US
dc.contributor.authorJacqueline Mickelsonen_US
dc.contributor.authorJoanne Van Rynen_US
dc.contributor.authorRobert P. Hebbelen_US
dc.contributor.authorDougald M. Monroeen_US
dc.contributor.authorNigel Mackmanen_US
dc.contributor.authorNigel S. Keyen_US
dc.contributor.authorRafal Pawlinskien_US
dc.contributor.otherThe University of North Carolina at Chapel Hillen_US
dc.contributor.otherMahidol Universityen_US
dc.contributor.otherBoehringer Ingelheim Pharma GmbH & Co. KGen_US
dc.contributor.otherUniversity of Minnesota Medical Schoolen_US
dc.date.accessioned2018-11-09T01:53:39Z-
dc.date.available2018-11-09T01:53:39Z-
dc.date.issued2014-03-13en_US
dc.identifier.citationBlood. Vol.123, No.11 (2014), 1747-1756en_US
dc.identifier.issn15280020en_US
dc.identifier.issn00064971en_US
dc.identifier.other2-s2.0-84897481862en_US
dc.identifier.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84897481862&origin=inwarden_US
dc.identifier.urihttp://repository.li.mahidol.ac.th/dspace/handle/123456789/33286-
dc.description.abstractActivation of coagulation and vascular inflammation are prominent features of sickle cell disease (SCD). Previously, we have shown that inhibition of tissue factor (TF) attenuates activation of coagulation and vascular inflammation in mouse models of SCD. In this study, we examined the mechanism by which coagulation proteases enhance vascular inflammation in sickle BERK mice. To specifically investigate the contribution of FXa and thrombin, mice were fed chow containing either rivaroxaban or dabigatran, respectively. In addition, we used bone marrow transplantation to generate sickle mice deficient in either protease activated receptor-1 (PAR-1) or protease activated receptor-2 (PAR-2) on nonhematopoietic cells. FXa inhibition and PAR-2 deficiency in nonhematopoietic cells attenuated systemic inflammation, measured by plasma levels of interleukin-6 (IL-6). In contrast, neither thrombin inhibition nor PAR-1 deficiency in nonhematopoietic cells affected plasma levels of IL-6 in sickle mice. However, thrombin did contribute to neutrophil infiltration in the lung, independently of PAR-1 expressed by nonhematopoietic cells. Furthermore, the TF-dependent increase in plasma levels of soluble vascular cell adhesion molecule-1 in sickle mice was not mediated by FXa or thrombin. Our data indicate that TF, FXa, and thrombin differentially contribute to vascular inflammation in a mouse model of SCD. © 2014 by The American Society of Hematology.en_US
dc.rightsMahidol Universityen_US
dc.source.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84897481862&origin=inwarden_US
dc.subjectBiochemistry, Genetics and Molecular Biologyen_US
dc.subjectImmunology and Microbiologyen_US
dc.subjectMedicineen_US
dc.titleDifferential contribution of FXa and thrombin to vascular inflammation in a mouse model of sickle cell diseaseen_US
dc.typeArticleen_US
dc.rights.holderSCOPUSen_US
dc.identifier.doi10.1182/blood-2013-08-523936en_US
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