Opposing roles of glucocorticoid receptor and mineralocorticoid receptor in trimethyltin-induced cytotoxicity in the mouse hippocampus

Autores
Ogita, Kiyokazu; Sugiyama, Chie; Acosta, Gabriela Beatriz; Kuramoto, Nobuyuki; Shuto, Makoto; Yoneyama, Masanori; Nakamura, Yukary; Shiba, Tatsuo; Yamaguchi, Taro
Año de publicación
2012
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
The organotin trimethyltin (TMT) is known to cause neuronal degeneration in the murine brain. Earlier studies indicate that TMT-induced neuronal degeneration is enhanced by adrenalectomy and prevented by exogenous glucocorticoid. The aim of this study was to investigate the regulation of TMT neuroxicity by corticosterone receptors including type I (mineralocorticoid receptor, MR) and type II (glucocorticoid receptor, GR) in adult mice. The systemic injection of TMT at the dose of 2.0 or 2.8. mg/kg produced a marked elevation in the level of plasma corticosterone that was both dose and time dependent. The MR agonist aldosterone had the ability to exacerbate TMT cytotoxicity in the dentate granule cell layer, whereas its antagonist spironolactone protected neurons from TMT cytotoxicity there. In contrast, the GR antagonist mifepristone exacerbated the TMT cytotoxicity. Taken together, our data suggest TMT cytotoxicity is oppositely regulated by GR and MR signals, being exacerbated by MR activation in adult mice. © 2012 Elsevier Ireland Ltd.
Fil: Ogita, Kiyokazu. Setsunan University; Japón
Fil: Sugiyama, Chie. Setsunan University; Japón
Fil: Acosta, Gabriela Beatriz. 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. Setsunan University; Japón
Fil: Kuramoto, Nobuyuki. Setsunan University; Japón
Fil: Shuto, Makoto. Setsunan University; Japón
Fil: Yoneyama, Masanori. Setsunan University; Japón
Fil: Nakamura, Yukary. Setsunan University; Japón
Fil: Shiba, Tatsuo. Setsunan University; Japón
Fil: Yamaguchi, Taro. Setsunan University; Japón
Materia
Glucocorticoid Receptor Hippocampus
Mineralocorticoid Receptor
Trimethyltin
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:11336/67494
Acceder
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network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Opposing roles of glucocorticoid receptor and mineralocorticoid receptor in trimethyltin-induced cytotoxicity in the mouse hippocampusOgita, KiyokazuSugiyama, ChieAcosta, Gabriela BeatrizKuramoto, NobuyukiShuto, MakotoYoneyama, MasanoriNakamura, YukaryShiba, TatsuoYamaguchi, TaroGlucocorticoid Receptor HippocampusMineralocorticoid ReceptorTrimethyltinhttps://purl.org/becyt/ford/3.3https://purl.org/becyt/ford/3The organotin trimethyltin (TMT) is known to cause neuronal degeneration in the murine brain. Earlier studies indicate that TMT-induced neuronal degeneration is enhanced by adrenalectomy and prevented by exogenous glucocorticoid. The aim of this study was to investigate the regulation of TMT neuroxicity by corticosterone receptors including type I (mineralocorticoid receptor, MR) and type II (glucocorticoid receptor, GR) in adult mice. The systemic injection of TMT at the dose of 2.0 or 2.8. mg/kg produced a marked elevation in the level of plasma corticosterone that was both dose and time dependent. The MR agonist aldosterone had the ability to exacerbate TMT cytotoxicity in the dentate granule cell layer, whereas its antagonist spironolactone protected neurons from TMT cytotoxicity there. In contrast, the GR antagonist mifepristone exacerbated the TMT cytotoxicity. Taken together, our data suggest TMT cytotoxicity is oppositely regulated by GR and MR signals, being exacerbated by MR activation in adult mice. © 2012 Elsevier Ireland Ltd.Fil: Ogita, Kiyokazu. Setsunan University; JapónFil: Sugiyama, Chie. Setsunan University; JapónFil: Acosta, Gabriela Beatriz. 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. Setsunan University; JapónFil: Kuramoto, Nobuyuki. Setsunan University; JapónFil: Shuto, Makoto. Setsunan University; JapónFil: Yoneyama, Masanori. Setsunan University; JapónFil: Nakamura, Yukary. Setsunan University; JapónFil: Shiba, Tatsuo. Setsunan University; JapónFil: Yamaguchi, Taro. Setsunan University; JapónElsevier Ireland2012-03info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/67494Ogita, Kiyokazu; Sugiyama, Chie; Acosta, Gabriela Beatriz; Kuramoto, Nobuyuki; Shuto, Makoto; et al.; Opposing roles of glucocorticoid receptor and mineralocorticoid receptor in trimethyltin-induced cytotoxicity in the mouse hippocampus; Elsevier Ireland; Neuroscience Letters; 511; 2; 3-2012; 116-1190304-3940CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1016/j.neulet.2012.01.052info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S0304394012001218info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:45:40Zoai:ri.conicet.gov.ar:11336/67494instacron: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 09:45:40.973CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Opposing roles of glucocorticoid receptor and mineralocorticoid receptor in trimethyltin-induced cytotoxicity in the mouse hippocampus
title Opposing roles of glucocorticoid receptor and mineralocorticoid receptor in trimethyltin-induced cytotoxicity in the mouse hippocampus
spellingShingle Opposing roles of glucocorticoid receptor and mineralocorticoid receptor in trimethyltin-induced cytotoxicity in the mouse hippocampus
Ogita, Kiyokazu
Glucocorticoid Receptor Hippocampus
Mineralocorticoid Receptor
Trimethyltin
title_short Opposing roles of glucocorticoid receptor and mineralocorticoid receptor in trimethyltin-induced cytotoxicity in the mouse hippocampus
title_full Opposing roles of glucocorticoid receptor and mineralocorticoid receptor in trimethyltin-induced cytotoxicity in the mouse hippocampus
title_fullStr Opposing roles of glucocorticoid receptor and mineralocorticoid receptor in trimethyltin-induced cytotoxicity in the mouse hippocampus
title_full_unstemmed Opposing roles of glucocorticoid receptor and mineralocorticoid receptor in trimethyltin-induced cytotoxicity in the mouse hippocampus
title_sort Opposing roles of glucocorticoid receptor and mineralocorticoid receptor in trimethyltin-induced cytotoxicity in the mouse hippocampus
dc.creator.none.fl_str_mv Ogita, Kiyokazu
Sugiyama, Chie
Acosta, Gabriela Beatriz
Kuramoto, Nobuyuki
Shuto, Makoto
Yoneyama, Masanori
Nakamura, Yukary
Shiba, Tatsuo
Yamaguchi, Taro
author Ogita, Kiyokazu
author_facet Ogita, Kiyokazu
Sugiyama, Chie
Acosta, Gabriela Beatriz
Kuramoto, Nobuyuki
Shuto, Makoto
Yoneyama, Masanori
Nakamura, Yukary
Shiba, Tatsuo
Yamaguchi, Taro
author_role author
author2 Sugiyama, Chie
Acosta, Gabriela Beatriz
Kuramoto, Nobuyuki
Shuto, Makoto
Yoneyama, Masanori
Nakamura, Yukary
Shiba, Tatsuo
Yamaguchi, Taro
author2_role author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Glucocorticoid Receptor Hippocampus
Mineralocorticoid Receptor
Trimethyltin
topic Glucocorticoid Receptor Hippocampus
Mineralocorticoid Receptor
Trimethyltin
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.3
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv The organotin trimethyltin (TMT) is known to cause neuronal degeneration in the murine brain. Earlier studies indicate that TMT-induced neuronal degeneration is enhanced by adrenalectomy and prevented by exogenous glucocorticoid. The aim of this study was to investigate the regulation of TMT neuroxicity by corticosterone receptors including type I (mineralocorticoid receptor, MR) and type II (glucocorticoid receptor, GR) in adult mice. The systemic injection of TMT at the dose of 2.0 or 2.8. mg/kg produced a marked elevation in the level of plasma corticosterone that was both dose and time dependent. The MR agonist aldosterone had the ability to exacerbate TMT cytotoxicity in the dentate granule cell layer, whereas its antagonist spironolactone protected neurons from TMT cytotoxicity there. In contrast, the GR antagonist mifepristone exacerbated the TMT cytotoxicity. Taken together, our data suggest TMT cytotoxicity is oppositely regulated by GR and MR signals, being exacerbated by MR activation in adult mice. © 2012 Elsevier Ireland Ltd.
Fil: Ogita, Kiyokazu. Setsunan University; Japón
Fil: Sugiyama, Chie. Setsunan University; Japón
Fil: Acosta, Gabriela Beatriz. 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. Setsunan University; Japón
Fil: Kuramoto, Nobuyuki. Setsunan University; Japón
Fil: Shuto, Makoto. Setsunan University; Japón
Fil: Yoneyama, Masanori. Setsunan University; Japón
Fil: Nakamura, Yukary. Setsunan University; Japón
Fil: Shiba, Tatsuo. Setsunan University; Japón
Fil: Yamaguchi, Taro. Setsunan University; Japón
description The organotin trimethyltin (TMT) is known to cause neuronal degeneration in the murine brain. Earlier studies indicate that TMT-induced neuronal degeneration is enhanced by adrenalectomy and prevented by exogenous glucocorticoid. The aim of this study was to investigate the regulation of TMT neuroxicity by corticosterone receptors including type I (mineralocorticoid receptor, MR) and type II (glucocorticoid receptor, GR) in adult mice. The systemic injection of TMT at the dose of 2.0 or 2.8. mg/kg produced a marked elevation in the level of plasma corticosterone that was both dose and time dependent. The MR agonist aldosterone had the ability to exacerbate TMT cytotoxicity in the dentate granule cell layer, whereas its antagonist spironolactone protected neurons from TMT cytotoxicity there. In contrast, the GR antagonist mifepristone exacerbated the TMT cytotoxicity. Taken together, our data suggest TMT cytotoxicity is oppositely regulated by GR and MR signals, being exacerbated by MR activation in adult mice. © 2012 Elsevier Ireland Ltd.
publishDate 2012
dc.date.none.fl_str_mv 2012-03
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/11336/67494
Ogita, Kiyokazu; Sugiyama, Chie; Acosta, Gabriela Beatriz; Kuramoto, Nobuyuki; Shuto, Makoto; et al.; Opposing roles of glucocorticoid receptor and mineralocorticoid receptor in trimethyltin-induced cytotoxicity in the mouse hippocampus; Elsevier Ireland; Neuroscience Letters; 511; 2; 3-2012; 116-119
0304-3940
CONICET Digital
CONICET
url http://hdl.handle.net/11336/67494
identifier_str_mv Ogita, Kiyokazu; Sugiyama, Chie; Acosta, Gabriela Beatriz; Kuramoto, Nobuyuki; Shuto, Makoto; et al.; Opposing roles of glucocorticoid receptor and mineralocorticoid receptor in trimethyltin-induced cytotoxicity in the mouse hippocampus; Elsevier Ireland; Neuroscience Letters; 511; 2; 3-2012; 116-119
0304-3940
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.1016/j.neulet.2012.01.052
info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S0304394012001218
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 Elsevier Ireland
publisher.none.fl_str_mv Elsevier Ireland
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 13.13397

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