Thyroid hormone receptor Beta1 gene expression is increased by dexamethasone at transcriptional level in rat liver

Autores
Montesinos, Maria del Mar; Pellizas, Claudia Gabriela; Velez, Maria Laura; Susperreguy, Sebastian; Masini, Ana Carla Ailín; Coleoni, Aldo Hector
Año de publicación
2006
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Triiodothyronine (T3) exerts most of its effect through nuclear thyroid hormone receptors (TR) which bind mainly as heterodimers with retinoid-X receptors (RXR) to thyroid hormone response elements (TRE) in target genes. It is well known that the synergistic interaction of T3 and glucocorticoids has a role on the synthesis of growth hormone in rat pituitary cell lines and in the T3-induced metamorphosis in amphibians. Glucocorticoids increased mRNAs of T3-regulated hepatic genes. Our laboratory reported increased specific metabolic actions of T3 in rat liver by Dexamethasone (Dex) through a mechanism involving an up-regulation of the maximal binding capacity of TR. In this study we further explored the participation of TR in the molecular mechanism of the Dex-induced increase on liver T3-specific metabolic action. Dex administration to adrenalectomized rats induced an increase of liver TRbeta1 protein and mRNA. Nuclear run-on assay revealed that Dex up-regulated the TR gene transcriptional rate. Transfection assay in COS-7 cells indicated that Dex increased the transcriptional activity of the TRbeta1 promoter. Electrophoretic mobility shift assay demonstrated that Dex induced the binding of additional proteins related to or neighboring the DNA sequence of a glucocorticoid receptor (GR) binding (GRE) half-site in the TRbeta1 promoter. Evidences for an interaction of GR on the TRbeta1 promoter have been obtained. Moreover, the specificity of the GR binding to GRE was determined not only by the GRE DNA sequence, but also by the interaction of the GR with other transacting factors bound to sequences flanking the GRE.
Fil: Montesinos, Maria del Mar. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones En Bioquímica Clínica E Inmunología; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Bioquímica Clínica; Argentina
Fil: Pellizas, Claudia Gabriela. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones En Bioquímica Clínica E Inmunología; Argentina. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Departamento de Bioquímica Clínica; Argentina
Fil: Velez, Maria Laura. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones En Bioquímica Clínica E Inmunología; Argentina. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Departamento de Bioquímica Clínica; Argentina
Fil: Susperreguy, Sebastian. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Departamento de Bioquímica Clínica; Argentina
Fil: Masini, Ana Carla Ailín. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones En Bioquímica Clínica E Inmunología; Argentina. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Departamento de Bioquímica Clínica; Argentina
Fil: Coleoni, Aldo Hector. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones En Bioquímica Clínica E Inmunología; Argentina. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Departamento de Bioquímica Clínica; Argentina
Materia
Thyroid Hormone
Transcriptional Regulation
Gene Expression
Molecular Secuence Data
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/18513
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/18513
network_acronym_str CONICETDig
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network_name_str CONICET Digital (CONICET)
spelling Thyroid hormone receptor Beta1 gene expression is increased by dexamethasone at transcriptional level in rat liverMontesinos, Maria del MarPellizas, Claudia GabrielaVelez, Maria LauraSusperreguy, SebastianMasini, Ana Carla AilínColeoni, Aldo HectorThyroid HormoneTranscriptional RegulationGene ExpressionMolecular Secuence Datahttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Triiodothyronine (T3) exerts most of its effect through nuclear thyroid hormone receptors (TR) which bind mainly as heterodimers with retinoid-X receptors (RXR) to thyroid hormone response elements (TRE) in target genes. It is well known that the synergistic interaction of T3 and glucocorticoids has a role on the synthesis of growth hormone in rat pituitary cell lines and in the T3-induced metamorphosis in amphibians. Glucocorticoids increased mRNAs of T3-regulated hepatic genes. Our laboratory reported increased specific metabolic actions of T3 in rat liver by Dexamethasone (Dex) through a mechanism involving an up-regulation of the maximal binding capacity of TR. In this study we further explored the participation of TR in the molecular mechanism of the Dex-induced increase on liver T3-specific metabolic action. Dex administration to adrenalectomized rats induced an increase of liver TRbeta1 protein and mRNA. Nuclear run-on assay revealed that Dex up-regulated the TR gene transcriptional rate. Transfection assay in COS-7 cells indicated that Dex increased the transcriptional activity of the TRbeta1 promoter. Electrophoretic mobility shift assay demonstrated that Dex induced the binding of additional proteins related to or neighboring the DNA sequence of a glucocorticoid receptor (GR) binding (GRE) half-site in the TRbeta1 promoter. Evidences for an interaction of GR on the TRbeta1 promoter have been obtained. Moreover, the specificity of the GR binding to GRE was determined not only by the GRE DNA sequence, but also by the interaction of the GR with other transacting factors bound to sequences flanking the GRE.Fil: Montesinos, Maria del Mar. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones En Bioquímica Clínica E Inmunología; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Bioquímica Clínica; ArgentinaFil: Pellizas, Claudia Gabriela. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones En Bioquímica Clínica E Inmunología; Argentina. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Departamento de Bioquímica Clínica; ArgentinaFil: Velez, Maria Laura. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones En Bioquímica Clínica E Inmunología; Argentina. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Departamento de Bioquímica Clínica; ArgentinaFil: Susperreguy, Sebastian. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Departamento de Bioquímica Clínica; ArgentinaFil: Masini, Ana Carla Ailín. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones En Bioquímica Clínica E Inmunología; Argentina. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Departamento de Bioquímica Clínica; ArgentinaFil: Coleoni, Aldo Hector. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones En Bioquímica Clínica E Inmunología; Argentina. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Departamento de Bioquímica Clínica; ArgentinaElsevier Inc2006-04-25info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/18513Montesinos, Maria del Mar; Pellizas, Claudia Gabriela; Velez, Maria Laura; Susperreguy, Sebastian; Masini, Ana Carla Ailín; et al.; Thyroid hormone receptor Beta1 gene expression is increased by dexamethasone at transcriptional level in rat liver; Elsevier Inc; Life Sciences; 78; 22; 25-4-2006; 2584-25940024-32050024-3205enginfo:eu-repo/semantics/altIdentifier/doi/10.1016/j.lfs.2005.10.019info:eu-repo/semantics/altIdentifier/url/http://www.sciencedirect.com/science/article/pii/S0024320505011355info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-nd/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:59:06Zoai:ri.conicet.gov.ar:11336/18513instacron: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 09:59:06.944CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Thyroid hormone receptor Beta1 gene expression is increased by dexamethasone at transcriptional level in rat liver
title Thyroid hormone receptor Beta1 gene expression is increased by dexamethasone at transcriptional level in rat liver
spellingShingle Thyroid hormone receptor Beta1 gene expression is increased by dexamethasone at transcriptional level in rat liver
Montesinos, Maria del Mar
Thyroid Hormone
Transcriptional Regulation
Gene Expression
Molecular Secuence Data
title_short Thyroid hormone receptor Beta1 gene expression is increased by dexamethasone at transcriptional level in rat liver
title_full Thyroid hormone receptor Beta1 gene expression is increased by dexamethasone at transcriptional level in rat liver
title_fullStr Thyroid hormone receptor Beta1 gene expression is increased by dexamethasone at transcriptional level in rat liver
title_full_unstemmed Thyroid hormone receptor Beta1 gene expression is increased by dexamethasone at transcriptional level in rat liver
title_sort Thyroid hormone receptor Beta1 gene expression is increased by dexamethasone at transcriptional level in rat liver
dc.creator.none.fl_str_mv Montesinos, Maria del Mar
Pellizas, Claudia Gabriela
Velez, Maria Laura
Susperreguy, Sebastian
Masini, Ana Carla Ailín
Coleoni, Aldo Hector
author Montesinos, Maria del Mar
author_facet Montesinos, Maria del Mar
Pellizas, Claudia Gabriela
Velez, Maria Laura
Susperreguy, Sebastian
Masini, Ana Carla Ailín
Coleoni, Aldo Hector
author_role author
author2 Pellizas, Claudia Gabriela
Velez, Maria Laura
Susperreguy, Sebastian
Masini, Ana Carla Ailín
Coleoni, Aldo Hector
author2_role author
author
author
author
author
dc.subject.none.fl_str_mv Thyroid Hormone
Transcriptional Regulation
Gene Expression
Molecular Secuence Data
topic Thyroid Hormone
Transcriptional Regulation
Gene Expression
Molecular Secuence Data
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Triiodothyronine (T3) exerts most of its effect through nuclear thyroid hormone receptors (TR) which bind mainly as heterodimers with retinoid-X receptors (RXR) to thyroid hormone response elements (TRE) in target genes. It is well known that the synergistic interaction of T3 and glucocorticoids has a role on the synthesis of growth hormone in rat pituitary cell lines and in the T3-induced metamorphosis in amphibians. Glucocorticoids increased mRNAs of T3-regulated hepatic genes. Our laboratory reported increased specific metabolic actions of T3 in rat liver by Dexamethasone (Dex) through a mechanism involving an up-regulation of the maximal binding capacity of TR. In this study we further explored the participation of TR in the molecular mechanism of the Dex-induced increase on liver T3-specific metabolic action. Dex administration to adrenalectomized rats induced an increase of liver TRbeta1 protein and mRNA. Nuclear run-on assay revealed that Dex up-regulated the TR gene transcriptional rate. Transfection assay in COS-7 cells indicated that Dex increased the transcriptional activity of the TRbeta1 promoter. Electrophoretic mobility shift assay demonstrated that Dex induced the binding of additional proteins related to or neighboring the DNA sequence of a glucocorticoid receptor (GR) binding (GRE) half-site in the TRbeta1 promoter. Evidences for an interaction of GR on the TRbeta1 promoter have been obtained. Moreover, the specificity of the GR binding to GRE was determined not only by the GRE DNA sequence, but also by the interaction of the GR with other transacting factors bound to sequences flanking the GRE.
Fil: Montesinos, Maria del Mar. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones En Bioquímica Clínica E Inmunología; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Bioquímica Clínica; Argentina
Fil: Pellizas, Claudia Gabriela. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones En Bioquímica Clínica E Inmunología; Argentina. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Departamento de Bioquímica Clínica; Argentina
Fil: Velez, Maria Laura. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones En Bioquímica Clínica E Inmunología; Argentina. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Departamento de Bioquímica Clínica; Argentina
Fil: Susperreguy, Sebastian. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Departamento de Bioquímica Clínica; Argentina
Fil: Masini, Ana Carla Ailín. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones En Bioquímica Clínica E Inmunología; Argentina. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Departamento de Bioquímica Clínica; Argentina
Fil: Coleoni, Aldo Hector. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones En Bioquímica Clínica E Inmunología; Argentina. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Departamento de Bioquímica Clínica; Argentina
description Triiodothyronine (T3) exerts most of its effect through nuclear thyroid hormone receptors (TR) which bind mainly as heterodimers with retinoid-X receptors (RXR) to thyroid hormone response elements (TRE) in target genes. It is well known that the synergistic interaction of T3 and glucocorticoids has a role on the synthesis of growth hormone in rat pituitary cell lines and in the T3-induced metamorphosis in amphibians. Glucocorticoids increased mRNAs of T3-regulated hepatic genes. Our laboratory reported increased specific metabolic actions of T3 in rat liver by Dexamethasone (Dex) through a mechanism involving an up-regulation of the maximal binding capacity of TR. In this study we further explored the participation of TR in the molecular mechanism of the Dex-induced increase on liver T3-specific metabolic action. Dex administration to adrenalectomized rats induced an increase of liver TRbeta1 protein and mRNA. Nuclear run-on assay revealed that Dex up-regulated the TR gene transcriptional rate. Transfection assay in COS-7 cells indicated that Dex increased the transcriptional activity of the TRbeta1 promoter. Electrophoretic mobility shift assay demonstrated that Dex induced the binding of additional proteins related to or neighboring the DNA sequence of a glucocorticoid receptor (GR) binding (GRE) half-site in the TRbeta1 promoter. Evidences for an interaction of GR on the TRbeta1 promoter have been obtained. Moreover, the specificity of the GR binding to GRE was determined not only by the GRE DNA sequence, but also by the interaction of the GR with other transacting factors bound to sequences flanking the GRE.
publishDate 2006
dc.date.none.fl_str_mv 2006-04-25
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/11336/18513
Montesinos, Maria del Mar; Pellizas, Claudia Gabriela; Velez, Maria Laura; Susperreguy, Sebastian; Masini, Ana Carla Ailín; et al.; Thyroid hormone receptor Beta1 gene expression is increased by dexamethasone at transcriptional level in rat liver; Elsevier Inc; Life Sciences; 78; 22; 25-4-2006; 2584-2594
0024-3205
0024-3205
url http://hdl.handle.net/11336/18513
identifier_str_mv Montesinos, Maria del Mar; Pellizas, Claudia Gabriela; Velez, Maria Laura; Susperreguy, Sebastian; Masini, Ana Carla Ailín; et al.; Thyroid hormone receptor Beta1 gene expression is increased by dexamethasone at transcriptional level in rat liver; Elsevier Inc; Life Sciences; 78; 22; 25-4-2006; 2584-2594
0024-3205
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.1016/j.lfs.2005.10.019
info:eu-repo/semantics/altIdentifier/url/http://www.sciencedirect.com/science/article/pii/S0024320505011355
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Elsevier Inc
publisher.none.fl_str_mv Elsevier 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 13.13397

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