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dc.contributor.authorNayernia, Zeynab
dc.contributor.authorColaianna, Marilena
dc.contributor.authorRobledinos-Antón, Natalia
dc.contributor.authorGutzwiller, Eveline
dc.contributor.authorSloan-Béna, Frédérique
dc.contributor.authorStathaki, Elisavet
dc.contributor.authorHibaoui, Yousef
dc.contributor.authorCuadrado Pastor, Antonio 
dc.contributor.authorHescheler, Jürgen
dc.contributor.authorStasia, Marie-José
dc.contributor.authorSaric, Tomo
dc.contributor.authorJaquet, Vincent
dc.contributor.authorKrause, Karl Heinz
dc.contributor.otherUAM. Departamento de Bioquímicaes_ES
dc.contributor.otherInstituto de Investigaciones Biomédicas "Alberto Sols" (IIBM)es_ES
dc.date.accessioned2017-11-29T15:43:56Z
dc.date.available2017-11-29T15:43:56Z
dc.date.issued2017-04-24
dc.identifier.citationRedox Biology 13 (2017): 82-93en_US
dc.identifier.issn2213-2317es_ES
dc.identifier.urihttp://hdl.handle.net/10486/680546
dc.description.abstractThere is emerging evidence for the involvement of reactive oxygen species (ROS) in the regulation of stem cells and cellular differentiation. Absence of the ROS-generating NADPH oxidase NOX2 in chronic granulomatous disease (CGD) patients, predominantly manifests as immune deficiency, but has also been associated with decreased cognition. Here, we investigate the role of NOX enzymes in neuronal homeostasis in adult mouse brain and in neural cells derived from human induced pluripotent stem cells (iPSC). High levels of NOX2 were found in mouse adult neurogenic regions. In NOX2-deficient mice, neurogenic regions showed diminished redox modifications, as well as decrease in neuroprecursor numbers and in expression of genes involved in neural differentiation including NES, BDNF and OTX2. iPSC from healthy subjects and patients with CGD were used to study the role of NOX2 in human in vitro neuronal development. Expression of NOX2 was low in undifferentiated iPSC, upregulated upon neural induction, and disappeared during neuronal differentiation. In human neurospheres, NOX2 protein and ROS generation were polarized within the inner cell layer of rosette structures. NOX2 deficiency in CGD-iPSCs resulted in an abnormal neural induction in vitro, as revealed by a reduced expression of neuroprogenitor markers (NES, BDNF, OTX2, NRSF/REST), and a decreased generation of mature neurons. Vector-mediated NOX2 expression in NOX2-deficient iPSCs rescued neurogenesis. Taken together, our study provides novel evidence for a regulatory role of NOX2 during early stages of neurogenesis in mouse and humanen_US
dc.description.sponsorshipThis study was supported by the Swiss National Foundation (SNF) grant number 31003A-160220/1, European Community's Framework Programme (FP7/2007–2013) under grant 278611 (Neurinox), Swiss State Secretariat for Education and Innovation C13.0142, German Federal Ministry for Education and Research (Bundesministerium (für Bildung und Forschung, BMBF; grant number 01GN0824), Ministry for Innovation, Science und Research of the State of North Rhine-Westphalia (323-400-010-13), and Köln Fortune Programs of the Medical Faculty of the University of Cologne, Germany. Natalia Robledinos-Anton was supported by a grant from the COST action EUROS BM1203 and the program for training university lecturers (FPU14/01073) from Spanish Ministry of Educationen_US
dc.format.extent12 pag.es_ES
dc.format.mimetypeapplication/pdfen
dc.language.isoengen
dc.publisherElsevier B.V.en_US
dc.relation.ispartofRedox Biologyen_US
dc.rights© 2017 The Authorsen_US
dc.subject.otherNOX2en_US
dc.subject.otherReactive oxygen speciesen_US
dc.subject.otherAdult neurogenesis in vitro neural differentiationen_US
dc.subject.otherNeural stem/progenitor cellsen_US
dc.subject.otherInduced pluripotent stem cells (iPSC)en_US
dc.titleDecreased neural precursor cell pool in NADPH oxidase 2-deficiency: From mouse brain to neural differentiation of patient derived iPSCen_US
dc.typearticleen
dc.subject.ecienciaMedicinaes_ES
dc.relation.publisherversionhttp://dx.doi.org/10.1016/j.redox.2017.04.026en
dc.identifier.doi10.1016/j.redox.2017.04.026es_ES
dc.identifier.publicationfirstpage82es_ES
dc.identifier.publicationlastpage93es_ES
dc.identifier.publicationvolume13es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/EC/H2020/1203/EU//COSTen
dc.relation.projectIDinfo:eu-repo/grant/Agreement/EC/FP7/278611en
dc.type.versioninfo:eu-repo/semantics/publishedVersionen
dc.rights.ccReconocimiento – NoComercial – SinObraDerivadaes_ES
dc.rights.accessRightsopenAccessen
dc.authorUAMRobledinos Antón, Natalia (271160)
dc.facultadUAMFacultad de Medicina
dc.institutoUAMInstituto de Investigaciones Biomédicas "Alberto Sols" (IIBM)


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