CD44 expression in the cuprizone model.
CD44
Cuprizone
Demyelination
Immunohistochemistry
Multiple sclerosis
Journal
Brain research
ISSN: 1872-6240
Titre abrégé: Brain Res
Pays: Netherlands
ID NLM: 0045503
Informations de publication
Date de publication:
15 10 2020
15 10 2020
Historique:
received:
14
01
2020
revised:
08
05
2020
accepted:
05
06
2020
pubmed:
12
6
2020
medline:
5
10
2021
entrez:
12
6
2020
Statut:
ppublish
Résumé
Numerous studies report that changes in extracellular matrix components and receptors, such as CD44, contribute to immune cell recruitment and thus lesion formation in multiple sclerosis (MS). In the present study, we used the cuprizone model to elucidate the expression pattern of CD44 in a toxin-induced MS model. Therefore, tissues of cuprizone-intoxicated mice were analyzed by real-time qRT-PCR and immunohistochemical staining against CD44. Co-localization analyses of CD44-positive cells with glial cell markers were performed by immunofluorescence labeling and in-situ hybridization. To investigate the functional importance of CD44 expression for myelination and glial cell activation, Cd44-deficient mice were used. In this study we demonstrate that CD44 expression is induced in a time-dependent manner in an autoimmune-independent model of MS. Up-regulation of CD44 expression was primarily associated to the superficial and perivascular glia limitans and demyelinated white matter structures, particularly the corpus callosum. In the demyelinated corpus callosum, CD44 was localized on GFAP
Identifiants
pubmed: 32524994
pii: S0006-8993(20)30306-1
doi: 10.1016/j.brainres.2020.146950
pii:
doi:
Substances chimiques
Cd44 protein, mouse
0
Chelating Agents
0
Hyaluronan Receptors
0
Cuprizone
5N16U7E0AO
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
146950Informations de copyright
Copyright © 2020. Published by Elsevier B.V.
Déclaration de conflit d'intérêts
Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.