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
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/98716
Ver los metadatos del registro completo
id |
CONICETDig_7440dc5dd7cc5f647b6b577f5e62c233 |
---|---|
oai_identifier_str |
oai:ri.conicet.gov.ar:11336/98716 |
network_acronym_str |
CONICETDig |
repository_id_str |
3498 |
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 |
dc.relation.none.fl_str_mv |
info:eu-repo/semantics/altIdentifier/url/https://onlinelibrary.wiley.com/doi/full/10.1111/jnc.12748 info:eu-repo/semantics/altIdentifier/doi/10.1111/jnc.12748 |
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 |
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) |
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 |
_version_ |
1842269640816852992 |
score |
13.13397 |