Astroglial phenotypes in traumatic brain injury and their relationship with neuronal degeneration
- Autores
- Cieri, M. B.; Mailing, Ingrid Eleonora; Villarreal, Alejandro; Ramos, Alberto Javier
- Año de publicación
- 2020
- Idioma
- inglés
- Tipo de recurso
- documento de conferencia
- Estado
- versión publicada
- Descripción
- Astrocytes are key players in the Central Nervous System injury.By not completely defined pathways, reactive astrocytes may suffer a pathological remodeling engaging a pro-inflammatory phenotype that is very stable and promote further neuroinflammation andneurodegeneration. We here aimed to define the spatio-temporaldistribution of astroglial phenotypes after traumatic brain injury andthe consequences for neuronal survival and behavioral parameters.Following a stereotaxic stab wound injury (0.8 mm needle, coordinates 2 mm posterior and lateral to Bregma; 1 mm depth) performedin C57BL/6 mice and immunohistochemistry on brain sections, weclassified GFAP reactive astrocytes in five different phenotypes defined using Sholl analysis (Auzmendi et al., Molec. Neurobiol. 2019).While at 1 day post-injury (DPI) GFAP+ astrocytes were not differentfrom contralateral non-injured hemisphere, at 3DPI and 7DPI highly reactive phenotypes colocalized with altered neurons in lesionpenumbra. At 14DPI highly reactive astrocytes and altered neuronswere abundant only in the lesion core. Pro-inflammatory gain offunction paradigm was achieved by administering LPS (5 mg/Kg i.p)in lesioned animals, and that resulted in a greater number of complex reactive astrocytes at 7DPI (p<0.05) and a population of C3+astrocytes. On the other hand, loss of function paradigm with chemical NFkB blocker sulfasalazine (150 mg/kg i.p) significantly reducedhighly reactive astrocytes (p<0.05) and showed reduced neuronaldeath. Animal motor deficits were analyzed by computer-assistedopen field, but at 7DPI we were unable to detect significative differences among groups probably due to the small lesion size. Weconclude that increased GFAP+ higher complexity astrocytes areassociated with increased neuronal death and that NFkB pathway islikely to be involved in the pathological conversion to the pro-inflammatory-neurodegenerative phenotype.
Fil: Cieri, M. B.. 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: Mailing, Ingrid Eleonora. 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: 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
LXV Reunión anual de la Sociedad Argentina de Investigación Clínica; LXVIII Reunión anual de la Sociedad Argentina de Inmunología y Reunión Anual de la Asociación Argentina de Fisiología
Argentina
Sociedad Argentina de Investigación Clínica
Sociedad Argentina de Inmunología
Asociación Argentina de Fisiología - Materia
-
ASTROCYTES
PHENOTYPES
TRAUMATIC BRAIN INJURY - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
- Repositorio
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/199441
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Astroglial phenotypes in traumatic brain injury and their relationship with neuronal degenerationCieri, M. B.Mailing, Ingrid EleonoraVillarreal, AlejandroRamos, Alberto JavierASTROCYTESPHENOTYPESTRAUMATIC BRAIN INJURYhttps://purl.org/becyt/ford/3.3https://purl.org/becyt/ford/3Astrocytes are key players in the Central Nervous System injury.By not completely defined pathways, reactive astrocytes may suffer a pathological remodeling engaging a pro-inflammatory phenotype that is very stable and promote further neuroinflammation andneurodegeneration. We here aimed to define the spatio-temporaldistribution of astroglial phenotypes after traumatic brain injury andthe consequences for neuronal survival and behavioral parameters.Following a stereotaxic stab wound injury (0.8 mm needle, coordinates 2 mm posterior and lateral to Bregma; 1 mm depth) performedin C57BL/6 mice and immunohistochemistry on brain sections, weclassified GFAP reactive astrocytes in five different phenotypes defined using Sholl analysis (Auzmendi et al., Molec. Neurobiol. 2019).While at 1 day post-injury (DPI) GFAP+ astrocytes were not differentfrom contralateral non-injured hemisphere, at 3DPI and 7DPI highly reactive phenotypes colocalized with altered neurons in lesionpenumbra. At 14DPI highly reactive astrocytes and altered neuronswere abundant only in the lesion core. Pro-inflammatory gain offunction paradigm was achieved by administering LPS (5 mg/Kg i.p)in lesioned animals, and that resulted in a greater number of complex reactive astrocytes at 7DPI (p<0.05) and a population of C3+astrocytes. On the other hand, loss of function paradigm with chemical NFkB blocker sulfasalazine (150 mg/kg i.p) significantly reducedhighly reactive astrocytes (p<0.05) and showed reduced neuronaldeath. Animal motor deficits were analyzed by computer-assistedopen field, but at 7DPI we were unable to detect significative differences among groups probably due to the small lesion size. Weconclude that increased GFAP+ higher complexity astrocytes areassociated with increased neuronal death and that NFkB pathway islikely to be involved in the pathological conversion to the pro-inflammatory-neurodegenerative phenotype.Fil: Cieri, M. B.. 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: Mailing, Ingrid Eleonora. 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: 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; ArgentinaLXV Reunión anual de la Sociedad Argentina de Investigación Clínica; LXVIII Reunión anual de la Sociedad Argentina de Inmunología y Reunión Anual de la Asociación Argentina de FisiologíaArgentinaSociedad Argentina de Investigación ClínicaSociedad Argentina de InmunologíaAsociación Argentina de FisiologíaFundación Revista Medicina2020info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/conferenceObjectReuniónJournalhttp://purl.org/coar/resource_type/c_5794info:ar-repo/semantics/documentoDeConferenciaapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/199441Astroglial phenotypes in traumatic brain injury and their relationship with neuronal degeneration; LXV Reunión anual de la Sociedad Argentina de Investigación Clínica; LXVIII Reunión anual de la Sociedad Argentina de Inmunología y Reunión Anual de la Asociación Argentina de Fisiología; Argentina; 2020; 106-1060025-7680CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.saic.org.ar/reunion-anualNacionalinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:52:08Zoai:ri.conicet.gov.ar:11336/199441instacron: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:34982025-09-03 09:52:08.59CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
dc.title.none.fl_str_mv |
Astroglial phenotypes in traumatic brain injury and their relationship with neuronal degeneration |
title |
Astroglial phenotypes in traumatic brain injury and their relationship with neuronal degeneration |
spellingShingle |
Astroglial phenotypes in traumatic brain injury and their relationship with neuronal degeneration Cieri, M. B. ASTROCYTES PHENOTYPES TRAUMATIC BRAIN INJURY |
title_short |
Astroglial phenotypes in traumatic brain injury and their relationship with neuronal degeneration |
title_full |
Astroglial phenotypes in traumatic brain injury and their relationship with neuronal degeneration |
title_fullStr |
Astroglial phenotypes in traumatic brain injury and their relationship with neuronal degeneration |
title_full_unstemmed |
Astroglial phenotypes in traumatic brain injury and their relationship with neuronal degeneration |
title_sort |
Astroglial phenotypes in traumatic brain injury and their relationship with neuronal degeneration |
dc.creator.none.fl_str_mv |
Cieri, M. B. Mailing, Ingrid Eleonora Villarreal, Alejandro Ramos, Alberto Javier |
author |
Cieri, M. B. |
author_facet |
Cieri, M. B. Mailing, Ingrid Eleonora Villarreal, Alejandro Ramos, Alberto Javier |
author_role |
author |
author2 |
Mailing, Ingrid Eleonora Villarreal, Alejandro Ramos, Alberto Javier |
author2_role |
author author author |
dc.subject.none.fl_str_mv |
ASTROCYTES PHENOTYPES TRAUMATIC BRAIN INJURY |
topic |
ASTROCYTES PHENOTYPES TRAUMATIC BRAIN INJURY |
purl_subject.fl_str_mv |
https://purl.org/becyt/ford/3.3 https://purl.org/becyt/ford/3 |
dc.description.none.fl_txt_mv |
Astrocytes are key players in the Central Nervous System injury.By not completely defined pathways, reactive astrocytes may suffer a pathological remodeling engaging a pro-inflammatory phenotype that is very stable and promote further neuroinflammation andneurodegeneration. We here aimed to define the spatio-temporaldistribution of astroglial phenotypes after traumatic brain injury andthe consequences for neuronal survival and behavioral parameters.Following a stereotaxic stab wound injury (0.8 mm needle, coordinates 2 mm posterior and lateral to Bregma; 1 mm depth) performedin C57BL/6 mice and immunohistochemistry on brain sections, weclassified GFAP reactive astrocytes in five different phenotypes defined using Sholl analysis (Auzmendi et al., Molec. Neurobiol. 2019).While at 1 day post-injury (DPI) GFAP+ astrocytes were not differentfrom contralateral non-injured hemisphere, at 3DPI and 7DPI highly reactive phenotypes colocalized with altered neurons in lesionpenumbra. At 14DPI highly reactive astrocytes and altered neuronswere abundant only in the lesion core. Pro-inflammatory gain offunction paradigm was achieved by administering LPS (5 mg/Kg i.p)in lesioned animals, and that resulted in a greater number of complex reactive astrocytes at 7DPI (p<0.05) and a population of C3+astrocytes. On the other hand, loss of function paradigm with chemical NFkB blocker sulfasalazine (150 mg/kg i.p) significantly reducedhighly reactive astrocytes (p<0.05) and showed reduced neuronaldeath. Animal motor deficits were analyzed by computer-assistedopen field, but at 7DPI we were unable to detect significative differences among groups probably due to the small lesion size. Weconclude that increased GFAP+ higher complexity astrocytes areassociated with increased neuronal death and that NFkB pathway islikely to be involved in the pathological conversion to the pro-inflammatory-neurodegenerative phenotype. Fil: Cieri, M. B.. 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: Mailing, Ingrid Eleonora. 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: 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 LXV Reunión anual de la Sociedad Argentina de Investigación Clínica; LXVIII Reunión anual de la Sociedad Argentina de Inmunología y Reunión Anual de la Asociación Argentina de Fisiología Argentina Sociedad Argentina de Investigación Clínica Sociedad Argentina de Inmunología Asociación Argentina de Fisiología |
description |
Astrocytes are key players in the Central Nervous System injury.By not completely defined pathways, reactive astrocytes may suffer a pathological remodeling engaging a pro-inflammatory phenotype that is very stable and promote further neuroinflammation andneurodegeneration. We here aimed to define the spatio-temporaldistribution of astroglial phenotypes after traumatic brain injury andthe consequences for neuronal survival and behavioral parameters.Following a stereotaxic stab wound injury (0.8 mm needle, coordinates 2 mm posterior and lateral to Bregma; 1 mm depth) performedin C57BL/6 mice and immunohistochemistry on brain sections, weclassified GFAP reactive astrocytes in five different phenotypes defined using Sholl analysis (Auzmendi et al., Molec. Neurobiol. 2019).While at 1 day post-injury (DPI) GFAP+ astrocytes were not differentfrom contralateral non-injured hemisphere, at 3DPI and 7DPI highly reactive phenotypes colocalized with altered neurons in lesionpenumbra. At 14DPI highly reactive astrocytes and altered neuronswere abundant only in the lesion core. Pro-inflammatory gain offunction paradigm was achieved by administering LPS (5 mg/Kg i.p)in lesioned animals, and that resulted in a greater number of complex reactive astrocytes at 7DPI (p<0.05) and a population of C3+astrocytes. On the other hand, loss of function paradigm with chemical NFkB blocker sulfasalazine (150 mg/kg i.p) significantly reducedhighly reactive astrocytes (p<0.05) and showed reduced neuronaldeath. Animal motor deficits were analyzed by computer-assistedopen field, but at 7DPI we were unable to detect significative differences among groups probably due to the small lesion size. Weconclude that increased GFAP+ higher complexity astrocytes areassociated with increased neuronal death and that NFkB pathway islikely to be involved in the pathological conversion to the pro-inflammatory-neurodegenerative phenotype. |
publishDate |
2020 |
dc.date.none.fl_str_mv |
2020 |
dc.type.none.fl_str_mv |
info:eu-repo/semantics/publishedVersion info:eu-repo/semantics/conferenceObject Reunión Journal http://purl.org/coar/resource_type/c_5794 info:ar-repo/semantics/documentoDeConferencia |
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publishedVersion |
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conferenceObject |
dc.identifier.none.fl_str_mv |
http://hdl.handle.net/11336/199441 Astroglial phenotypes in traumatic brain injury and their relationship with neuronal degeneration; LXV Reunión anual de la Sociedad Argentina de Investigación Clínica; LXVIII Reunión anual de la Sociedad Argentina de Inmunología y Reunión Anual de la Asociación Argentina de Fisiología; Argentina; 2020; 106-106 0025-7680 CONICET Digital CONICET |
url |
http://hdl.handle.net/11336/199441 |
identifier_str_mv |
Astroglial phenotypes in traumatic brain injury and their relationship with neuronal degeneration; LXV Reunión anual de la Sociedad Argentina de Investigación Clínica; LXVIII Reunión anual de la Sociedad Argentina de Inmunología y Reunión Anual de la Asociación Argentina de Fisiología; Argentina; 2020; 106-106 0025-7680 CONICET Digital CONICET |
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eng |
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eng |
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Fundación Revista Medicina |
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Fundación Revista Medicina |
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dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar |
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