NGF controls dendrite development in hippocampal neurons by binding to p75NTR and modulating the cellular targets of Notch

Notch and neurotrophins control neuronal shape, but it is not known whether their signaling pathways intersect. Here we report results from hippocampal neuronal cultures that are in support of this possibility. We found that low cell density or blockade of Notch signaling by a soluble Delta-Fc ligan...

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Autores: Salama-Cohen, P., Arévalo, María Ángeles, Meier, J., Grantyn, R., Rodríguez-Tebar, Alfredo
Formato: artículo
Fecha de publicación:2005
País:España
Recursos:Consejo Superior de Investigaciones Científicas (CSIC)
Repositorio:DIGITAL.CSIC. Repositorio Institucional del CSIC
OAI Identifier:oai:digital.csic.es:10261/150408
Acesso em linha:http://hdl.handle.net/10261/150408
Access Level:acceso abierto
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spelling NGF controls dendrite development in hippocampal neurons by binding to p75NTR and modulating the cellular targets of NotchSalama-Cohen, P.Arévalo, María ÁngelesMeier, J.Grantyn, R.Rodríguez-Tebar, AlfredoNotch and neurotrophins control neuronal shape, but it is not known whether their signaling pathways intersect. Here we report results from hippocampal neuronal cultures that are in support of this possibility. We found that low cell density or blockade of Notch signaling by a soluble Delta-Fc ligand decreased the mRNA levels of the nuclear targets of Notch, the homologues of enhancer-of-split 1 and 5 (Hes1/5). This effect was associated with enhanced sprouting of new dendrites or dendrite branches. In contrast, high cell density or exposure of low-density cultures to NGF increased the Hes1/5 mRNA, reduced the number of primary dendrites and promoted dendrite elongation. The NGF effects on both Hes1/5 expression and dendrite morphology were prevented by p75-antibody (a p75NTR-blocking antibody) or transfection with enhancer-of-split 6 (Hes6), a condition known to suppress Hes activity. Nuclear translocation of NF-kappaB was identified as a link between p75NTR and Hes1/5 because it was required for the up-regulation of these two genes. The convergence of the Notch and p75NTR signaling pathways at the level of Hes1/5 illuminates an unexpected mechanism through which a diffusible factor (NGF) could regulate dendrite growth when cell-cell interaction via Notch is not in action.Peer ReviewedAmerican Society for Cell BiologyConsejo Superior de Investigaciones Científicas [https://ror.org/02gfc7t72]2017201720052017info:eu-repo/semantics/articlehttp://purl.org/coar/resource_type/c_6501http://hdl.handle.net/10261/150408reponame:DIGITAL.CSIC. Repositorio Institucional del CSICinstname:Consejo Superior de Investigaciones Científicas (CSIC)InglésSíinfo:eu-repo/semantics/openAccessoai:digital.csic.es:10261/1504082026-05-22T06:33:51Z
dc.title.none.fl_str_mv NGF controls dendrite development in hippocampal neurons by binding to p75NTR and modulating the cellular targets of Notch
title NGF controls dendrite development in hippocampal neurons by binding to p75NTR and modulating the cellular targets of Notch
spellingShingle NGF controls dendrite development in hippocampal neurons by binding to p75NTR and modulating the cellular targets of Notch
Salama-Cohen, P.
title_short NGF controls dendrite development in hippocampal neurons by binding to p75NTR and modulating the cellular targets of Notch
title_full NGF controls dendrite development in hippocampal neurons by binding to p75NTR and modulating the cellular targets of Notch
title_fullStr NGF controls dendrite development in hippocampal neurons by binding to p75NTR and modulating the cellular targets of Notch
title_full_unstemmed NGF controls dendrite development in hippocampal neurons by binding to p75NTR and modulating the cellular targets of Notch
title_sort NGF controls dendrite development in hippocampal neurons by binding to p75NTR and modulating the cellular targets of Notch
dc.creator.none.fl_str_mv Salama-Cohen, P.
Arévalo, María Ángeles
Meier, J.
Grantyn, R.
Rodríguez-Tebar, Alfredo
author Salama-Cohen, P.
author_facet Salama-Cohen, P.
Arévalo, María Ángeles
Meier, J.
Grantyn, R.
Rodríguez-Tebar, Alfredo
author_role author
author2 Arévalo, María Ángeles
Meier, J.
Grantyn, R.
Rodríguez-Tebar, Alfredo
author2_role author
author
author
author
dc.contributor.none.fl_str_mv Consejo Superior de Investigaciones Científicas [https://ror.org/02gfc7t72]
description Notch and neurotrophins control neuronal shape, but it is not known whether their signaling pathways intersect. Here we report results from hippocampal neuronal cultures that are in support of this possibility. We found that low cell density or blockade of Notch signaling by a soluble Delta-Fc ligand decreased the mRNA levels of the nuclear targets of Notch, the homologues of enhancer-of-split 1 and 5 (Hes1/5). This effect was associated with enhanced sprouting of new dendrites or dendrite branches. In contrast, high cell density or exposure of low-density cultures to NGF increased the Hes1/5 mRNA, reduced the number of primary dendrites and promoted dendrite elongation. The NGF effects on both Hes1/5 expression and dendrite morphology were prevented by p75-antibody (a p75NTR-blocking antibody) or transfection with enhancer-of-split 6 (Hes6), a condition known to suppress Hes activity. Nuclear translocation of NF-kappaB was identified as a link between p75NTR and Hes1/5 because it was required for the up-regulation of these two genes. The convergence of the Notch and p75NTR signaling pathways at the level of Hes1/5 illuminates an unexpected mechanism through which a diffusible factor (NGF) could regulate dendrite growth when cell-cell interaction via Notch is not in action.
publishDate 2005
dc.date.none.fl_str_mv 2005
2017
2017
2017
dc.type.none.fl_str_mv info:eu-repo/semantics/article
http://purl.org/coar/resource_type/c_6501
format article
dc.identifier.none.fl_str_mv http://hdl.handle.net/10261/150408
url http://hdl.handle.net/10261/150408
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.relation.none.fl_str_mv
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.publisher.none.fl_str_mv American Society for Cell Biology
publisher.none.fl_str_mv American Society for Cell Biology
dc.source.none.fl_str_mv reponame:DIGITAL.CSIC. Repositorio Institucional del CSIC
instname:Consejo Superior de Investigaciones Científicas (CSIC)
instname_str Consejo Superior de Investigaciones Científicas (CSIC)
reponame_str DIGITAL.CSIC. Repositorio Institucional del CSIC
collection DIGITAL.CSIC. Repositorio Institucional del CSIC
repository.name.fl_str_mv
repository.mail.fl_str_mv
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