S100β as an early biomarker of excitotoxic damage in spinal cord organotypic cultures

Autores
Mazzone, Graciela Luján; Nistri, Andrea
Año de publicación
2014
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
S100β is a cytoplasmic calcium‐binding protein mainly expressed by glia and considered to be a useful biomarker for brain or spinal cord injury. Indeed, clinical studies suggest that the S100β concentration in serum or cerebrospinal fluid may predict lesion outcome and prognosis. The relation of S100β levels to damage severity and its timecourse remains, however, unclear. This study used a validated in vitro model of spinal cord injury induced by kainate‐mediated excitotoxicity to investigate these issues. After 22 days in vitro, rat organotypic spinal cord slices were subjected to one transient application (1 h) of 1 or 100 μM kainate followed by washout. While the lower kainate concentration did not evoke neuronal loss or S100β increase, the larger concentration elicited 40% neuronal death, no change in glial number and a delayed, significant rise in extracellular S100β that peaked at 24 h. This increase was associated with a stronger expression of the S100β protein as indicated by western blotting and immunohistochemistry. Application of the microtubule disrupting agent colchicine did not change the rise in S100β induced by kainate, an effect blocked by the glutamate receptor antagonists CNQX and APV. Our data suggest that excitotoxicity was followed by release of S100β perhaps from a readily releasable pool through a mechanism independent of microtubule assembly. The raised extracellular level of S100β appeared to reflect glial reactivity to the kainate‐evoked lesion in accordance with the view that this protein may be involved in tissue protection and repair after acute injury.
Fil: Mazzone, Graciela Luján. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. International School for Advanced Studies; Italia
Fil: Nistri, Andrea. International School for Advanced Studies; Italia
Materia
COLCHICINE
GLUTAMATE RECEPTOR
KAINIC ACID
NEUROPROTECTION
SPINAL CORD INJURY
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:11336/98716

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network_name_str CONICET Digital (CONICET)
spelling S100β as an early biomarker of excitotoxic damage in spinal cord organotypic culturesMazzone, Graciela LujánNistri, AndreaCOLCHICINEGLUTAMATE RECEPTORKAINIC ACIDNEUROPROTECTIONSPINAL CORD INJURYhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3S100β is a cytoplasmic calcium‐binding protein mainly expressed by glia and considered to be a useful biomarker for brain or spinal cord injury. Indeed, clinical studies suggest that the S100β concentration in serum or cerebrospinal fluid may predict lesion outcome and prognosis. The relation of S100β levels to damage severity and its timecourse remains, however, unclear. This study used a validated in vitro model of spinal cord injury induced by kainate‐mediated excitotoxicity to investigate these issues. After 22 days in vitro, rat organotypic spinal cord slices were subjected to one transient application (1 h) of 1 or 100 μM kainate followed by washout. While the lower kainate concentration did not evoke neuronal loss or S100β increase, the larger concentration elicited 40% neuronal death, no change in glial number and a delayed, significant rise in extracellular S100β that peaked at 24 h. This increase was associated with a stronger expression of the S100β protein as indicated by western blotting and immunohistochemistry. Application of the microtubule disrupting agent colchicine did not change the rise in S100β induced by kainate, an effect blocked by the glutamate receptor antagonists CNQX and APV. Our data suggest that excitotoxicity was followed by release of S100β perhaps from a readily releasable pool through a mechanism independent of microtubule assembly. The raised extracellular level of S100β appeared to reflect glial reactivity to the kainate‐evoked lesion in accordance with the view that this protein may be involved in tissue protection and repair after acute injury.Fil: Mazzone, Graciela Luján. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. International School for Advanced Studies; ItaliaFil: Nistri, Andrea. International School for Advanced Studies; ItaliaWiley Blackwell Publishing, Inc2014-05info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/98716Mazzone, Graciela Luján; Nistri, Andrea; S100β as an early biomarker of excitotoxic damage in spinal cord organotypic cultures; Wiley Blackwell Publishing, Inc; Journal of Neurochemistry; 130; 4; 5-2014; 598-6040022-3042CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://onlinelibrary.wiley.com/doi/full/10.1111/jnc.12748info:eu-repo/semantics/altIdentifier/doi/10.1111/jnc.12748info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T10:00:29Zoai:ri.conicet.gov.ar:11336/98716instacron: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 10:00:29.5CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv S100β as an early biomarker of excitotoxic damage in spinal cord organotypic cultures
title S100β as an early biomarker of excitotoxic damage in spinal cord organotypic cultures
spellingShingle S100β as an early biomarker of excitotoxic damage in spinal cord organotypic cultures
Mazzone, Graciela Luján
COLCHICINE
GLUTAMATE RECEPTOR
KAINIC ACID
NEUROPROTECTION
SPINAL CORD INJURY
title_short S100β as an early biomarker of excitotoxic damage in spinal cord organotypic cultures
title_full S100β as an early biomarker of excitotoxic damage in spinal cord organotypic cultures
title_fullStr S100β as an early biomarker of excitotoxic damage in spinal cord organotypic cultures
title_full_unstemmed S100β as an early biomarker of excitotoxic damage in spinal cord organotypic cultures
title_sort S100β as an early biomarker of excitotoxic damage in spinal cord organotypic cultures
dc.creator.none.fl_str_mv Mazzone, Graciela Luján
Nistri, Andrea
author Mazzone, Graciela Luján
author_facet Mazzone, Graciela Luján
Nistri, Andrea
author_role author
author2 Nistri, Andrea
author2_role author
dc.subject.none.fl_str_mv COLCHICINE
GLUTAMATE RECEPTOR
KAINIC ACID
NEUROPROTECTION
SPINAL CORD INJURY
topic COLCHICINE
GLUTAMATE RECEPTOR
KAINIC ACID
NEUROPROTECTION
SPINAL CORD INJURY
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv S100β is a cytoplasmic calcium‐binding protein mainly expressed by glia and considered to be a useful biomarker for brain or spinal cord injury. Indeed, clinical studies suggest that the S100β concentration in serum or cerebrospinal fluid may predict lesion outcome and prognosis. The relation of S100β levels to damage severity and its timecourse remains, however, unclear. This study used a validated in vitro model of spinal cord injury induced by kainate‐mediated excitotoxicity to investigate these issues. After 22 days in vitro, rat organotypic spinal cord slices were subjected to one transient application (1 h) of 1 or 100 μM kainate followed by washout. While the lower kainate concentration did not evoke neuronal loss or S100β increase, the larger concentration elicited 40% neuronal death, no change in glial number and a delayed, significant rise in extracellular S100β that peaked at 24 h. This increase was associated with a stronger expression of the S100β protein as indicated by western blotting and immunohistochemistry. Application of the microtubule disrupting agent colchicine did not change the rise in S100β induced by kainate, an effect blocked by the glutamate receptor antagonists CNQX and APV. Our data suggest that excitotoxicity was followed by release of S100β perhaps from a readily releasable pool through a mechanism independent of microtubule assembly. The raised extracellular level of S100β appeared to reflect glial reactivity to the kainate‐evoked lesion in accordance with the view that this protein may be involved in tissue protection and repair after acute injury.
Fil: Mazzone, Graciela Luján. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. International School for Advanced Studies; Italia
Fil: Nistri, Andrea. International School for Advanced Studies; Italia
description S100β is a cytoplasmic calcium‐binding protein mainly expressed by glia and considered to be a useful biomarker for brain or spinal cord injury. Indeed, clinical studies suggest that the S100β concentration in serum or cerebrospinal fluid may predict lesion outcome and prognosis. The relation of S100β levels to damage severity and its timecourse remains, however, unclear. This study used a validated in vitro model of spinal cord injury induced by kainate‐mediated excitotoxicity to investigate these issues. After 22 days in vitro, rat organotypic spinal cord slices were subjected to one transient application (1 h) of 1 or 100 μM kainate followed by washout. While the lower kainate concentration did not evoke neuronal loss or S100β increase, the larger concentration elicited 40% neuronal death, no change in glial number and a delayed, significant rise in extracellular S100β that peaked at 24 h. This increase was associated with a stronger expression of the S100β protein as indicated by western blotting and immunohistochemistry. Application of the microtubule disrupting agent colchicine did not change the rise in S100β induced by kainate, an effect blocked by the glutamate receptor antagonists CNQX and APV. Our data suggest that excitotoxicity was followed by release of S100β perhaps from a readily releasable pool through a mechanism independent of microtubule assembly. The raised extracellular level of S100β appeared to reflect glial reactivity to the kainate‐evoked lesion in accordance with the view that this protein may be involved in tissue protection and repair after acute injury.
publishDate 2014
dc.date.none.fl_str_mv 2014-05
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/11336/98716
Mazzone, Graciela Luján; Nistri, Andrea; S100β as an early biomarker of excitotoxic damage in spinal cord organotypic cultures; Wiley Blackwell Publishing, Inc; Journal of Neurochemistry; 130; 4; 5-2014; 598-604
0022-3042
CONICET Digital
CONICET
url http://hdl.handle.net/11336/98716
identifier_str_mv Mazzone, Graciela Luján; Nistri, Andrea; S100β as an early biomarker of excitotoxic damage in spinal cord organotypic cultures; Wiley Blackwell Publishing, Inc; Journal of Neurochemistry; 130; 4; 5-2014; 598-604
0022-3042
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
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info:eu-repo/semantics/altIdentifier/doi/10.1111/jnc.12748
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rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Wiley Blackwell Publishing, Inc
publisher.none.fl_str_mv Wiley Blackwell Publishing, Inc
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
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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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