Excess iodide downregulates Na+/I− symporter gene transcription through activation of PI3K/Akt pathway

Autores
Serrano Nascimento, Caroline; Nicola, Juan Pablo; da Silva Teixeira, Silvania; Poyares, Leonice Lourenço; Lellis Santos, Camilo; Bordin, Silvana; Masini, Ana María; Nunes, Maria Tereza
Año de publicación
2016
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Transcriptional mechanisms associated with iodide-induced downregulation of NIS expression remain uncertain. Here, we further analyzed the transcriptional regulation of NIS gene expression by excess iodide using PCCl3 cells. NIS promoter activity was reduced in cells treated for 12-24 h with 10-5 to 10-3 M NaI. Site-directed mutagenesis of Pax8 and NF-κB cis-acting elements abrogated the iodide-induced NIS transcription repression. Indeed, excess iodide (10-3M) excluded Pax8 from the nucleus, decreased p65 total expression and reduced their transcriptional activity. Importantly, p65-Pax8 physical interaction and binding to NIS upstream enhancer were reduced upon iodide treatment. PI3K/Akt pathway activation by iodide-induced ROS production is involved in the transcriptional repression of NIS expression. In conclusion, the results indicated that excess iodide transcriptionally represses NIS gene expression through the impairment of Pax8 and p65 transcriptional activity. Furthermore, the data presented herein described novel roles for PI3K/Akt signaling pathway and oxidative status in the thyroid autoregulatory phenomenon.
Fil: Serrano Nascimento, Caroline. Universidade de Sao Paulo; Brasil
Fil: Nicola, Juan Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
Fil: da Silva Teixeira, Silvania. Universidade de Sao Paulo; Brasil
Fil: Poyares, Leonice Lourenço. Universidade de Sao Paulo; Brasil
Fil: Lellis Santos, Camilo. Universidade de Sao Paulo; Brasil
Fil: Bordin, Silvana. Universidade de Sao Paulo; Brasil
Fil: Masini, Ana María. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
Fil: Nunes, Maria Tereza. Universidade de Sao Paulo; Brasil
Materia
Excess Iodide
Na+/I- Symporter
Reactive Oxygen Species
Pi3k/Akt Pathway
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:11336/46658
Acceder
id CONICETDig_5e5eb2fbc22649a52ca0b1d1052fddd7
oai_identifier_str oai:ri.conicet.gov.ar:11336/46658
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Excess iodide downregulates Na+/I− symporter gene transcription through activation of PI3K/Akt pathwaySerrano Nascimento, CarolineNicola, Juan Pabloda Silva Teixeira, SilvaniaPoyares, Leonice LourençoLellis Santos, CamiloBordin, SilvanaMasini, Ana MaríaNunes, Maria TerezaExcess IodideNa+/I- SymporterReactive Oxygen SpeciesPi3k/Akt Pathwayhttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Transcriptional mechanisms associated with iodide-induced downregulation of NIS expression remain uncertain. Here, we further analyzed the transcriptional regulation of NIS gene expression by excess iodide using PCCl3 cells. NIS promoter activity was reduced in cells treated for 12-24 h with 10<sup>-5</sup> to 10<sup>-3</sup> M NaI. Site-directed mutagenesis of Pax8 and NF-κB cis-acting elements abrogated the iodide-induced NIS transcription repression. Indeed, excess iodide (10<sup>-3</sup>M) excluded Pax8 from the nucleus, decreased p65 total expression and reduced their transcriptional activity. Importantly, p65-Pax8 physical interaction and binding to NIS upstream enhancer were reduced upon iodide treatment. PI3K/Akt pathway activation by iodide-induced ROS production is involved in the transcriptional repression of NIS expression. In conclusion, the results indicated that excess iodide transcriptionally represses NIS gene expression through the impairment of Pax8 and p65 transcriptional activity. Furthermore, the data presented herein described novel roles for PI3K/Akt signaling pathway and oxidative status in the thyroid autoregulatory phenomenon.Fil: Serrano Nascimento, Caroline. Universidade de Sao Paulo; BrasilFil: Nicola, Juan Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; ArgentinaFil: da Silva Teixeira, Silvania. Universidade de Sao Paulo; BrasilFil: Poyares, Leonice Lourenço. Universidade de Sao Paulo; BrasilFil: Lellis Santos, Camilo. Universidade de Sao Paulo; BrasilFil: Bordin, Silvana. Universidade de Sao Paulo; BrasilFil: Masini, Ana María. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; ArgentinaFil: Nunes, Maria Tereza. Universidade de Sao Paulo; BrasilElsevier Ireland2016-05info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/46658Serrano Nascimento, Caroline; Nicola, Juan Pablo; da Silva Teixeira, Silvania; Poyares, Leonice Lourenço; Lellis Santos, Camilo; et al.; Excess iodide downregulates Na+/I− symporter gene transcription through activation of PI3K/Akt pathway; Elsevier Ireland; Molecular and Cellular Endocrinology; 426; 5-2016; 73-900303-7207CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1016/j.mce.2016.02.006info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S0303720716300338info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-15T14:31:00Zoai:ri.conicet.gov.ar:11336/46658instacron: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:34982025-10-15 14:31:00.413CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Excess iodide downregulates Na+/I− symporter gene transcription through activation of PI3K/Akt pathway
title Excess iodide downregulates Na+/I− symporter gene transcription through activation of PI3K/Akt pathway
spellingShingle Excess iodide downregulates Na+/I− symporter gene transcription through activation of PI3K/Akt pathway
Serrano Nascimento, Caroline
Excess Iodide
Na+/I- Symporter
Reactive Oxygen Species
Pi3k/Akt Pathway
title_short Excess iodide downregulates Na+/I− symporter gene transcription through activation of PI3K/Akt pathway
title_full Excess iodide downregulates Na+/I− symporter gene transcription through activation of PI3K/Akt pathway
title_fullStr Excess iodide downregulates Na+/I− symporter gene transcription through activation of PI3K/Akt pathway
title_full_unstemmed Excess iodide downregulates Na+/I− symporter gene transcription through activation of PI3K/Akt pathway
title_sort Excess iodide downregulates Na+/I− symporter gene transcription through activation of PI3K/Akt pathway
dc.creator.none.fl_str_mv Serrano Nascimento, Caroline
Nicola, Juan Pablo
da Silva Teixeira, Silvania
Poyares, Leonice Lourenço
Lellis Santos, Camilo
Bordin, Silvana
Masini, Ana María
Nunes, Maria Tereza
author Serrano Nascimento, Caroline
author_facet Serrano Nascimento, Caroline
Nicola, Juan Pablo
da Silva Teixeira, Silvania
Poyares, Leonice Lourenço
Lellis Santos, Camilo
Bordin, Silvana
Masini, Ana María
Nunes, Maria Tereza
author_role author
author2 Nicola, Juan Pablo
da Silva Teixeira, Silvania
Poyares, Leonice Lourenço
Lellis Santos, Camilo
Bordin, Silvana
Masini, Ana María
Nunes, Maria Tereza
author2_role author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Excess Iodide
Na+/I- Symporter
Reactive Oxygen Species
Pi3k/Akt Pathway
topic Excess Iodide
Na+/I- Symporter
Reactive Oxygen Species
Pi3k/Akt Pathway
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv Transcriptional mechanisms associated with iodide-induced downregulation of NIS expression remain uncertain. Here, we further analyzed the transcriptional regulation of NIS gene expression by excess iodide using PCCl3 cells. NIS promoter activity was reduced in cells treated for 12-24 h with 10<sup>-5</sup> to 10<sup>-3</sup> M NaI. Site-directed mutagenesis of Pax8 and NF-κB cis-acting elements abrogated the iodide-induced NIS transcription repression. Indeed, excess iodide (10<sup>-3</sup>M) excluded Pax8 from the nucleus, decreased p65 total expression and reduced their transcriptional activity. Importantly, p65-Pax8 physical interaction and binding to NIS upstream enhancer were reduced upon iodide treatment. PI3K/Akt pathway activation by iodide-induced ROS production is involved in the transcriptional repression of NIS expression. In conclusion, the results indicated that excess iodide transcriptionally represses NIS gene expression through the impairment of Pax8 and p65 transcriptional activity. Furthermore, the data presented herein described novel roles for PI3K/Akt signaling pathway and oxidative status in the thyroid autoregulatory phenomenon.
Fil: Serrano Nascimento, Caroline. Universidade de Sao Paulo; Brasil
Fil: Nicola, Juan Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
Fil: da Silva Teixeira, Silvania. Universidade de Sao Paulo; Brasil
Fil: Poyares, Leonice Lourenço. Universidade de Sao Paulo; Brasil
Fil: Lellis Santos, Camilo. Universidade de Sao Paulo; Brasil
Fil: Bordin, Silvana. Universidade de Sao Paulo; Brasil
Fil: Masini, Ana María. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
Fil: Nunes, Maria Tereza. Universidade de Sao Paulo; Brasil
description Transcriptional mechanisms associated with iodide-induced downregulation of NIS expression remain uncertain. Here, we further analyzed the transcriptional regulation of NIS gene expression by excess iodide using PCCl3 cells. NIS promoter activity was reduced in cells treated for 12-24 h with 10<sup>-5</sup> to 10<sup>-3</sup> M NaI. Site-directed mutagenesis of Pax8 and NF-κB cis-acting elements abrogated the iodide-induced NIS transcription repression. Indeed, excess iodide (10<sup>-3</sup>M) excluded Pax8 from the nucleus, decreased p65 total expression and reduced their transcriptional activity. Importantly, p65-Pax8 physical interaction and binding to NIS upstream enhancer were reduced upon iodide treatment. PI3K/Akt pathway activation by iodide-induced ROS production is involved in the transcriptional repression of NIS expression. In conclusion, the results indicated that excess iodide transcriptionally represses NIS gene expression through the impairment of Pax8 and p65 transcriptional activity. Furthermore, the data presented herein described novel roles for PI3K/Akt signaling pathway and oxidative status in the thyroid autoregulatory phenomenon.
publishDate 2016
dc.date.none.fl_str_mv 2016-05
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/11336/46658
Serrano Nascimento, Caroline; Nicola, Juan Pablo; da Silva Teixeira, Silvania; Poyares, Leonice Lourenço; Lellis Santos, Camilo; et al.; Excess iodide downregulates Na+/I− symporter gene transcription through activation of PI3K/Akt pathway; Elsevier Ireland; Molecular and Cellular Endocrinology; 426; 5-2016; 73-90
0303-7207
CONICET Digital
CONICET
url http://hdl.handle.net/11336/46658
identifier_str_mv Serrano Nascimento, Caroline; Nicola, Juan Pablo; da Silva Teixeira, Silvania; Poyares, Leonice Lourenço; Lellis Santos, Camilo; et al.; Excess iodide downregulates Na+/I− symporter gene transcription through activation of PI3K/Akt pathway; Elsevier Ireland; Molecular and Cellular Endocrinology; 426; 5-2016; 73-90
0303-7207
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.mce.2016.02.006
info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S0303720716300338
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
_version_ 1846082790145130496
score 13.22299

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