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Blood-brain barrier hyperpermeability precedes demyelination in the cuprizone model

dc.contributor.authorBerghoff, Stefan A.
dc.contributor.authorDüking, Tim
dc.contributor.authorSpieth, Lena
dc.contributor.authorWinchenbach, Jan
dc.contributor.authorStumpf, Sina K.
dc.contributor.authorGerndt, Nina
dc.contributor.authorKusch, Kathrin
dc.contributor.authorRuhwedel, Torben
dc.contributor.authorMöbius, Wiebke
dc.contributor.authorSaher, Gesine
dc.date.accessioned2019-12-17T09:57:16Z
dc.date.available2019-12-17T09:57:16Z
dc.date.issued2017de
dc.relation.ISSN2051-5960de
dc.identifier.urihttp://resolver.sub.uni-goettingen.de/purl?gs-1/16992
dc.description.abstractIn neuroinflammatory disorders such as multiple sclerosis, the physiological function of the blood-brain barrier (BBB) is perturbed, particularly in demyelinating lesions and supposedly secondary to acute demyelinating pathology. Using the toxic non-inflammatory cuprizone model of demyelination, we demonstrate, however, that the onset of persistent BBB impairment precedes demyelination. In addition to a direct effect of cuprizone on endothelial cells, a plethora of inflammatory mediators, which are mainly of astroglial origin during the initial disease phase, likely contribute to the destabilization of endothelial barrier function in vivo. Our study reveals that, at different time points of pathology and in different CNS regions, the level of gliosis correlates with the extent of BBB hyperpermeability and edema. Furthermore, in mutant mice with abolished type 3 CXC chemokine receptor (CXCR3) signaling, inflammatory responses are dampened and BBB dysfunction ameliorated. Together, these data have implications for understanding the role of BBB permeability in the pathogenesis of demyelinating disease.de
dc.language.isoengde
dc.rightsopenAccess
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.subjectAstrocyte; Blood-brain barrier; Demyelination; Gliosis; Inflammatory mediatorsde
dc.subject.ddc573
dc.subject.ddc612
dc.titleBlood-brain barrier hyperpermeability precedes demyelination in the cuprizone modelde
dc.typejournalArticlede
dc.identifier.doi10.1186/s40478-017-0497-6
dc.type.versionpublishedVersionde
dc.relation.eISSN2051-5960
dc.bibliographicCitation.volume5de
dc.bibliographicCitation.issue1de
dc.type.subtypejournalArticle
dc.identifier.pmid29195512
dc.bibliographicCitation.articlenumber94de
dc.description.statuspeerReviewedde
dc.bibliographicCitation.journalActa Neuropathologica Communicationsde


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