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Inflammation Promotes a Conversion of Astrocytes into Neural Progenitor Cells via NF-κB Activation

dc.rights.licenseCC6en_US
dc.contributor.authorGabel, Sébastien
dc.contributor.authorKoncina, Eric
dc.contributor.authorDorban, Gauthier
dc.contributor.authorHeurtaux, Tony
dc.contributor.authorBirck, Cindy
dc.contributor.authorGlaab, Enrico
dc.contributor.authorMichelucci, Alessandro
dc.contributor.authorHeuschling, Paul
dc.contributor.authorGrandbarbe, Luc
dc.date.accessioned2020-09-25T12:23:44Z
dc.date.available2020-09-25T12:23:44Z
dc.date.issued2016-10
dc.identifier.issn0893-7648en_US
dc.identifier.urihttps://luck.synhera.be/handle/123456789/302
dc.identifier.doi10.1007/s12035-015-9428-3en_US
dc.description.abstractPublication traitant de la dédifférenciation des astrocytes dans un environnement inflammatoireen_US
dc.description.abstractenBrain inflammation, a common feature in neurodegenerative diseases, is a complex series of events, which can be detrimental and even lead to neuronal death. Nonetheless, several studies suggest that inflammatory signals are also positively influencing neural cell proliferation, survival, migration, and differentiation. Recently, correlative studies suggested that astrocytes are able to dedifferentiate upon injury and may thereby re-acquire neural stem cell (NSC) potential. However, the mechanism underlying this dedifferentiation process upon injury remains unclear. Here, we report that during the early response of reactive gliosis, inflammation induces a conversion of mature astrocytes into neural progenitors. A TNF treatment induces the decrease of specific astrocyte markers, such as glial fibrillary acidic protein (GFAP) or genes related to glycogen metabolism, while a subset of these cells re-expresses immaturity markers, such as CD44, Musashi-1, and Oct4. Thus, TNF treatment results in the appearance of cells that exhibit a neural progenitor phenotype and are able to proliferate and differentiate into neurons and/or astrocytes. This dedifferentiation process is maintained as long as TNF is present in the culture medium. In addition, we highlight a role for Oct4 in this process, since the TNF-induced dedifferentiation can be prevented by inhibiting Oct4 expression. Our results show that activation of the NF-κB pathway through TNF plays an important role in the dedifferentiation of astrocytes via the re-expression of Oct4. These findings indicate that the first step of reactive gliosis is in fact a dedifferentiation process of resident astrocytes mediated by the NF-κB pathway.en_US
dc.description.sponsorshipOTHen_US
dc.language.isoENen_US
dc.publisherSpringeren_US
dc.relation.ispartofMolecular Neurobiologyen_US
dc.rights.urihttps://creativecommons.org/licenses/by-nc/4.0/en_US
dc.subjectAstrocyteen_US
dc.subjectInflammationen_US
dc.subjectNF-κBen_US
dc.subjectNeural progenitor cellsen_US
dc.subject.enAstrocyteen_US
dc.subject.enInflammationen_US
dc.subject.enNF-KBen_US
dc.subject.enDedifferentiationen_US
dc.subject.enNeural Progenitor Cellsen_US
dc.titleInflammation Promotes a Conversion of Astrocytes into Neural Progenitor Cells via NF-κB Activationen_US
dc.title.enInflammation Promotes a Conversion of Astrocytes into Neural Progenitor Cells via NF-κB Activationen_US
dc.title.frL'inflammation induit la transformation des astrocytes en précurseurs neuronaux par l'activation de NF-KBen_US
dc.typeArticle scientifiqueen_US
synhera.classificationSciences de la santé humaineen_US
synhera.classificationSciences du vivanten_US
synhera.classificationSciences de la santé humaine>>Orthopédie, rééducation & médecine sportiveen_US
synhera.institutionHE Robert Schumanen_US
synhera.otherinstitutionUniversity of Luxembourgen_US
synhera.cost.total0en_US
synhera.cost.apc0en_US
synhera.cost.comp0en_US
synhera.cost.acccomp0en_US
dc.description.versionOuien_US
dc.rights.holderUniversity of Luxembourgen_US


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