p75 NTR expression is induced in isolated neurons of the penumbra after ischemia by cortical devascularization

Autores
Angelo, María Florencia; Aviles Reyes, Rolando Xavier; Villarreal, Alejandro; Barker, Philip A.; Reines, Analia Gabriela; Ramos, Alberto Javier
Año de publicación
2009
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
The p75 neurotrophin receptor (p75NTR) is involved in neuronal functions going from induction of apoptosis and growth inhibition to the promotion of survival. p75NTR expression is induced in central nervous system (CNS) by a wide range of pathological conditions where it seems to have a main role in neuronal death and axonal growth inhibition. The cellular mechanisms driving p75NTR expression in cell lines and primary neurons in culture depend on Sp1-induced transcription (Ramos et al., 2007, J. Neurosci 27:1498). In this study we analyzed the spatio-temporal profile of p75NTR expression after a localized ischemic lesion in the rat brain induced by cortical devascularization (CD). Our results showed that p75NTR expression occurred in isolated neurons of the ischemic penumbra. The p75NTR+ neurons presented morphological alterations and active caspase-3 staining. Some of these p75NTR+ neurons were also positive for sortilin. The peak of p75NTR expression was localized 3 days after the lesion (3DPL), while abundance of Sp1 transcription factor increased from 3 to 14DPL on the lesioned hemisphere. In primary cortical neurons, we demonstrated that p75NTR expression is induced by excitotoxic stress and correlated with increased Sp1 abundance. We conclude that p75NTR expression is localized in selected neurons of the ischemic penumbra and these neurons are probably condemned to apoptotic cell death. In primary neuronal culture is clear that excitotoxity and Sp1 are involved in induction of p75NTR expression, although in vivo some additional mechanisms are likely to be involved in the control of the p75NTR expression in specific neurons in vivo.
Fil: Angelo, María Florencia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Biología Celular y Neurociencia "Prof. Eduardo de Robertis". Universidad de Buenos Aires. Facultad de Medicina. Instituto de Biología Celular y Neurociencia; Argentina
Fil: Aviles Reyes, Rolando Xavier. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Biología Celular y Neurociencia "Prof. Eduardo de Robertis". Universidad de Buenos Aires. Facultad de Medicina. Instituto de Biología Celular y Neurociencia; Argentina
Fil: Villarreal, Alejandro. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Biología Celular y Neurociencia "Prof. Eduardo de Robertis". Universidad de Buenos Aires. Facultad de Medicina. Instituto de Biología Celular y Neurociencia; Argentina
Fil: Barker, Philip A.. McGill University; Canadá
Fil: Reines, Analia Gabriela. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Farmacológicas. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Investigaciones Farmacológicas; Argentina
Fil: Ramos, Alberto Javier. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Biología Celular y Neurociencia "Prof. Eduardo de Robertis". Universidad de Buenos Aires. Facultad de Medicina. Instituto de Biología Celular y Neurociencia; Argentina
Materia
GLUTAMATE
ISCHEMIA
NEURONAL DEATH
NEUROTROPHIN
SORTILIN
SP1
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/132828
Acceder
id CONICETDig_6c061830176fbd3f492f4179a9b061cb
oai_identifier_str oai:ri.conicet.gov.ar:11336/132828
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling p75 NTR expression is induced in isolated neurons of the penumbra after ischemia by cortical devascularizationAngelo, María FlorenciaAviles Reyes, Rolando XavierVillarreal, AlejandroBarker, Philip A.Reines, Analia GabrielaRamos, Alberto JavierGLUTAMATEISCHEMIANEURONAL DEATHNEUROTROPHINSORTILINSP1https://purl.org/becyt/ford/3.5https://purl.org/becyt/ford/3The p75 neurotrophin receptor (p75NTR) is involved in neuronal functions going from induction of apoptosis and growth inhibition to the promotion of survival. p75NTR expression is induced in central nervous system (CNS) by a wide range of pathological conditions where it seems to have a main role in neuronal death and axonal growth inhibition. The cellular mechanisms driving p75NTR expression in cell lines and primary neurons in culture depend on Sp1-induced transcription (Ramos et al., 2007, J. Neurosci 27:1498). In this study we analyzed the spatio-temporal profile of p75NTR expression after a localized ischemic lesion in the rat brain induced by cortical devascularization (CD). Our results showed that p75NTR expression occurred in isolated neurons of the ischemic penumbra. The p75NTR+ neurons presented morphological alterations and active caspase-3 staining. Some of these p75NTR+ neurons were also positive for sortilin. The peak of p75NTR expression was localized 3 days after the lesion (3DPL), while abundance of Sp1 transcription factor increased from 3 to 14DPL on the lesioned hemisphere. In primary cortical neurons, we demonstrated that p75NTR expression is induced by excitotoxic stress and correlated with increased Sp1 abundance. We conclude that p75NTR expression is localized in selected neurons of the ischemic penumbra and these neurons are probably condemned to apoptotic cell death. In primary neuronal culture is clear that excitotoxity and Sp1 are involved in induction of p75NTR expression, although in vivo some additional mechanisms are likely to be involved in the control of the p75NTR expression in specific neurons in vivo.Fil: Angelo, María Florencia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Biología Celular y Neurociencia "Prof. Eduardo de Robertis". Universidad de Buenos Aires. Facultad de Medicina. Instituto de Biología Celular y Neurociencia; ArgentinaFil: Aviles Reyes, Rolando Xavier. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Biología Celular y Neurociencia "Prof. Eduardo de Robertis". Universidad de Buenos Aires. Facultad de Medicina. Instituto de Biología Celular y Neurociencia; ArgentinaFil: Villarreal, Alejandro. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Biología Celular y Neurociencia "Prof. Eduardo de Robertis". Universidad de Buenos Aires. Facultad de Medicina. Instituto de Biología Celular y Neurociencia; ArgentinaFil: Barker, Philip A.. McGill University; CanadáFil: Reines, Analia Gabriela. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Farmacológicas. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Investigaciones Farmacológicas; ArgentinaFil: Ramos, Alberto Javier. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Biología Celular y Neurociencia "Prof. Eduardo de Robertis". Universidad de Buenos Aires. Facultad de Medicina. Instituto de Biología Celular y Neurociencia; ArgentinaWiley-liss, div John Wiley & Sons Inc.2009-10info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/132828Angelo, María Florencia; Aviles Reyes, Rolando Xavier; Villarreal, Alejandro; Barker, Philip A.; Reines, Analia Gabriela; et al.; p75 NTR expression is induced in isolated neurons of the penumbra after ischemia by cortical devascularization; Wiley-liss, div John Wiley & Sons Inc.; Journal of Neuroscience Research; 87; 8; 10-2009; 1892-19030360-4012CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://onlinelibrary.wiley.com/doi/abs/10.1002/jnr.21993info:eu-repo/semantics/altIdentifier/doi/10.1002/jnr.21993info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T09:45:50Zoai:ri.conicet.gov.ar:11336/132828instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-29 09:45:50.359CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv p75 NTR expression is induced in isolated neurons of the penumbra after ischemia by cortical devascularization
title p75 NTR expression is induced in isolated neurons of the penumbra after ischemia by cortical devascularization
spellingShingle p75 NTR expression is induced in isolated neurons of the penumbra after ischemia by cortical devascularization
Angelo, María Florencia
GLUTAMATE
ISCHEMIA
NEURONAL DEATH
NEUROTROPHIN
SORTILIN
SP1
title_short p75 NTR expression is induced in isolated neurons of the penumbra after ischemia by cortical devascularization
title_full p75 NTR expression is induced in isolated neurons of the penumbra after ischemia by cortical devascularization
title_fullStr p75 NTR expression is induced in isolated neurons of the penumbra after ischemia by cortical devascularization
title_full_unstemmed p75 NTR expression is induced in isolated neurons of the penumbra after ischemia by cortical devascularization
title_sort p75 NTR expression is induced in isolated neurons of the penumbra after ischemia by cortical devascularization
dc.creator.none.fl_str_mv Angelo, María Florencia
Aviles Reyes, Rolando Xavier
Villarreal, Alejandro
Barker, Philip A.
Reines, Analia Gabriela
Ramos, Alberto Javier
author Angelo, María Florencia
author_facet Angelo, María Florencia
Aviles Reyes, Rolando Xavier
Villarreal, Alejandro
Barker, Philip A.
Reines, Analia Gabriela
Ramos, Alberto Javier
author_role author
author2 Aviles Reyes, Rolando Xavier
Villarreal, Alejandro
Barker, Philip A.
Reines, Analia Gabriela
Ramos, Alberto Javier
author2_role author
author
author
author
author
dc.subject.none.fl_str_mv GLUTAMATE
ISCHEMIA
NEURONAL DEATH
NEUROTROPHIN
SORTILIN
SP1
topic GLUTAMATE
ISCHEMIA
NEURONAL DEATH
NEUROTROPHIN
SORTILIN
SP1
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.5
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv The p75 neurotrophin receptor (p75NTR) is involved in neuronal functions going from induction of apoptosis and growth inhibition to the promotion of survival. p75NTR expression is induced in central nervous system (CNS) by a wide range of pathological conditions where it seems to have a main role in neuronal death and axonal growth inhibition. The cellular mechanisms driving p75NTR expression in cell lines and primary neurons in culture depend on Sp1-induced transcription (Ramos et al., 2007, J. Neurosci 27:1498). In this study we analyzed the spatio-temporal profile of p75NTR expression after a localized ischemic lesion in the rat brain induced by cortical devascularization (CD). Our results showed that p75NTR expression occurred in isolated neurons of the ischemic penumbra. The p75NTR+ neurons presented morphological alterations and active caspase-3 staining. Some of these p75NTR+ neurons were also positive for sortilin. The peak of p75NTR expression was localized 3 days after the lesion (3DPL), while abundance of Sp1 transcription factor increased from 3 to 14DPL on the lesioned hemisphere. In primary cortical neurons, we demonstrated that p75NTR expression is induced by excitotoxic stress and correlated with increased Sp1 abundance. We conclude that p75NTR expression is localized in selected neurons of the ischemic penumbra and these neurons are probably condemned to apoptotic cell death. In primary neuronal culture is clear that excitotoxity and Sp1 are involved in induction of p75NTR expression, although in vivo some additional mechanisms are likely to be involved in the control of the p75NTR expression in specific neurons in vivo.
Fil: Angelo, María Florencia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Biología Celular y Neurociencia "Prof. Eduardo de Robertis". Universidad de Buenos Aires. Facultad de Medicina. Instituto de Biología Celular y Neurociencia; Argentina
Fil: Aviles Reyes, Rolando Xavier. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Biología Celular y Neurociencia "Prof. Eduardo de Robertis". Universidad de Buenos Aires. Facultad de Medicina. Instituto de Biología Celular y Neurociencia; Argentina
Fil: Villarreal, Alejandro. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Biología Celular y Neurociencia "Prof. Eduardo de Robertis". Universidad de Buenos Aires. Facultad de Medicina. Instituto de Biología Celular y Neurociencia; Argentina
Fil: Barker, Philip A.. McGill University; Canadá
Fil: Reines, Analia Gabriela. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Farmacológicas. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Investigaciones Farmacológicas; Argentina
Fil: Ramos, Alberto Javier. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Biología Celular y Neurociencia "Prof. Eduardo de Robertis". Universidad de Buenos Aires. Facultad de Medicina. Instituto de Biología Celular y Neurociencia; Argentina
description The p75 neurotrophin receptor (p75NTR) is involved in neuronal functions going from induction of apoptosis and growth inhibition to the promotion of survival. p75NTR expression is induced in central nervous system (CNS) by a wide range of pathological conditions where it seems to have a main role in neuronal death and axonal growth inhibition. The cellular mechanisms driving p75NTR expression in cell lines and primary neurons in culture depend on Sp1-induced transcription (Ramos et al., 2007, J. Neurosci 27:1498). In this study we analyzed the spatio-temporal profile of p75NTR expression after a localized ischemic lesion in the rat brain induced by cortical devascularization (CD). Our results showed that p75NTR expression occurred in isolated neurons of the ischemic penumbra. The p75NTR+ neurons presented morphological alterations and active caspase-3 staining. Some of these p75NTR+ neurons were also positive for sortilin. The peak of p75NTR expression was localized 3 days after the lesion (3DPL), while abundance of Sp1 transcription factor increased from 3 to 14DPL on the lesioned hemisphere. In primary cortical neurons, we demonstrated that p75NTR expression is induced by excitotoxic stress and correlated with increased Sp1 abundance. We conclude that p75NTR expression is localized in selected neurons of the ischemic penumbra and these neurons are probably condemned to apoptotic cell death. In primary neuronal culture is clear that excitotoxity and Sp1 are involved in induction of p75NTR expression, although in vivo some additional mechanisms are likely to be involved in the control of the p75NTR expression in specific neurons in vivo.
publishDate 2009
dc.date.none.fl_str_mv 2009-10
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/132828
Angelo, María Florencia; Aviles Reyes, Rolando Xavier; Villarreal, Alejandro; Barker, Philip A.; Reines, Analia Gabriela; et al.; p75 NTR expression is induced in isolated neurons of the penumbra after ischemia by cortical devascularization; Wiley-liss, div John Wiley & Sons Inc.; Journal of Neuroscience Research; 87; 8; 10-2009; 1892-1903
0360-4012
CONICET Digital
CONICET
url http://hdl.handle.net/11336/132828
identifier_str_mv Angelo, María Florencia; Aviles Reyes, Rolando Xavier; Villarreal, Alejandro; Barker, Philip A.; Reines, Analia Gabriela; et al.; p75 NTR expression is induced in isolated neurons of the penumbra after ischemia by cortical devascularization; Wiley-liss, div John Wiley & Sons Inc.; Journal of Neuroscience Research; 87; 8; 10-2009; 1892-1903
0360-4012
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://onlinelibrary.wiley.com/doi/abs/10.1002/jnr.21993
info:eu-repo/semantics/altIdentifier/doi/10.1002/jnr.21993
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
application/pdf
application/pdf
application/pdf
dc.publisher.none.fl_str_mv Wiley-liss, div John Wiley & Sons Inc.
publisher.none.fl_str_mv Wiley-liss, div John Wiley & Sons Inc.
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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score 13.070432

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