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dc.contributor.authorQuintela López, Tania
dc.contributor.authorOrtiz Sanz, Carolina
dc.contributor.authorSerrano Regal, Mari Paz
dc.contributor.authorGaminde Blasco, Adhara Mikaela
dc.contributor.authorValero Gómez-Lobo, Jorge
dc.contributor.authorBaleriola, Jimena
dc.contributor.authorSánchez Gómez, María Victoria
dc.contributor.authorMatute Almau, Carlos José
dc.contributor.authorAlberdi Alfonso, Elena María
dc.date.accessioned2020-02-25T09:20:27Z
dc.date.available2020-02-25T09:20:27Z
dc.date.issued2019-06-06
dc.identifier.citationCell Death & Disease 10 : (2019) // Article ID UNSP 445es_ES
dc.identifier.issn2041-4889
dc.identifier.urihttp://hdl.handle.net/10810/41430
dc.description.abstractAlzheimer's disease (AD) is characterized by a progressive cognitive decline that correlates with the levels of amyloid beta-peptide (A beta) oligomers. Strong evidences connect changes of oligodendrocyte function with the onset of neurodegeneration in AD. However, the mechanisms controlling oligodendrocyte responses to A beta are still elusive. Here, we tested the role of A beta in oligodendrocyte differentiation, maturation, and survival in isolated oligodendrocytes and in organotypic cerebellar slices. We found that A beta peptides specifically induced local translation of 18.5-kDa myelin basic protein (MBP) isoform in distal cell processes concomitant with an increase of process complexity of MBPexpressing oligodendrocytes. A beta oligomers required integrin beta 1 receptor, Src-family kinase Fyn and Ca2+/CaMKII as effectors to modulate MBP protein expression. The pharmacological inhibition of Fyn kinase also attenuated oligodendrocyte differentiation and survival induced by A beta oligomers. Similarly, using ex vivo organotypic cerebellar slices A beta promoted MBP upregulation through Fyn kinase, and modulated oligodendrocyte population dynamics by inducing cell proliferation and differentiation. Importantly, application of A beta to cerebellar organotypic slices enhanced remyelination and oligodendrocyte lineage recovery in lysolecithin (LPC)-induced demyelination. These data reveal an important role of A beta in oligodendrocyte lineage function and maturation, which may be relevant to AD pathogenesis.es_ES
dc.description.sponsorshipThis study was supported by the Basque Government (fellowship to T.Q.-L.), University of the Basque Country (UPV/EHU; fellowship to C.O.-S.), CIBERNED and MINECO (fellowship to A.G.-B. FPU17/04891; M.P.S.-R. SAF2013-45084-R and SAF2016-75292-R). We thank S. Marcos, A. Martinez, and L. Escobar for technical assistance.es_ES
dc.language.isoenges_ES
dc.publisherNature Publishing Groupes_ES
dc.relationinfo:eu-repo/grantAgreement/MINECO/FPU17/04891es_ES
dc.relationinfo:eu-repo/grantAgreement/MINECO/SAF2013-45084-Res_ES
dc.relationinfo:eu-repo/grantAgreement/MINECO/SAF2016-75292-Res_ES
dc.rightsinfo:eu-repo/semantics/openAccesses_ES
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/es/*
dc.subjectmyelin basic-proteines_ES
dc.subjectalzheimers-diseasees_ES
dc.subjectamyloid hypothesises_ES
dc.subjectcns myelinationes_ES
dc.subjectcell-survivales_ES
dc.subjectwhite-matteres_ES
dc.subjectmicees_ES
dc.subjectdemyelinationes_ES
dc.subjectassociationes_ES
dc.subjectactivationes_ES
dc.titleA beta oligomers promote oligodendrocyte differentiation and maturation via integrin beta 1 and Fyn kinase signalinges_ES
dc.typeinfo:eu-repo/semantics/articlees_ES
dc.rights.holderThis article is licensed under a Creative Commons Attribution 4.0 International License. (CC BY 4.0)es_ES
dc.rights.holderAtribución 3.0 España*
dc.relation.publisherversionhttps://www.nature.com/articles/s41419-019-1636-8es_ES
dc.identifier.doi10.1038/s41419-019-1636-8
dc.departamentoesNeurocienciases_ES
dc.departamentoeuNeurozientziakes_ES


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This article is licensed under a Creative Commons Attribution 4.0 International License. (CC BY 4.0)
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