CFTR modulates RPS27 gene expression using chloride anion as signaling effector

Autores
Valdivieso, Ángel Gabriel; Mori, Consuelo; Clauzure, Mariángeles; Massip Copiz, María Macarena; Santa Coloma, Tomás Antonio
Año de publicación
2017
Idioma
inglés
Tipo de recurso
artículo
Estado
versión aceptada
Descripción
Fil: Valdivieso, Ángel Gabriel. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; Argentina
Fil: Valdivieso, Ángel Gabriel. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Mori, Consuelo. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; Argentina
Fil: Mori, Consuelo. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Clauzure, Mariángeles. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; Argentina
Fil: Clauzure, Mariángeles. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Massip Copiz, María Macarena. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; Argentina
Fil: Massip Copiz, María Macarena. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Santa Coloma, Tomás Antonio. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; Argentina
Fil: Santa Coloma, Tomás Antonio. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Abstract: In Cystic Fibrosis (CF), the impairment of the CFTR channel activity leads to a variety of alterations, including differential gene expression. However, the CFTR signaling mechanisms remain unclear. Recently, culturing IB3-1 CF cells under different intracellular Clconcentrations ([Cl- ]i), we observed several Cl- -dependent genes and further characterized one of them as RPS27. Thus, we hypothesized that Cl- might act as a signaling effector for CFTR signaling. Here, to test this idea, we study RPS27 expression in T84 cells modulating the CFTR activity by using CFTR inhibitors. First, we observed that incubation of T84 cells with increasing concentrations of the CFTR inhibitors CFTR(inh)-172 or GlyH-101 determined a progressive increase in the relative [Cl- ]i (using the Cl- fluorescent probe SPQ). The [Cl- ]i rise was concomitant with a dose-dependent down-regulation of RPS27. These results imply that CFTR inhibition produce Cl- accumulation and that RPS27 expression can be modulated by CFTR inhibition. Therefore, Cl- behaves as a signaling effector for CFTR in the modulation of RPS27 expression. In addition, the IL-1β receptor antagonist IL1RN or the JNK inhibitor SP600125, both restored the down-regulation of RPS27 induced by CFTRinh-172, implying a role of autocrine IL-1β and JNK signaling downstream of Cl- in RPS27 modulation.
Fuente
Archives of Biochemistry and Biophysics Vol. 633, 2017
Materia
REGULADOR DE CONDUCTANCIA DE TRANSMEMBRANA DE FIBROSIS QUISTICA
PROTEINA RIBOSOMICA 40S S27
FIBROSIS QUISTICA
CLORURO
GENES
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/4.0/
Repositorio
Repositorio Institucional (UCA)
Institución
Pontificia Universidad Católica Argentina
OAI Identificador
oai:ucacris:123456789/14560
Acceder
id RIUCA_47c6ac03d2e193f5cfe98f504e0b912f
oai_identifier_str oai:ucacris:123456789/14560
network_acronym_str RIUCA
repository_id_str 2585
network_name_str Repositorio Institucional (UCA)
spelling CFTR modulates RPS27 gene expression using chloride anion as signaling effectorValdivieso, Ángel GabrielMori, ConsueloClauzure, MariángelesMassip Copiz, María MacarenaSanta Coloma, Tomás AntonioREGULADOR DE CONDUCTANCIA DE TRANSMEMBRANA DE FIBROSIS QUISTICAPROTEINA RIBOSOMICA 40S S27FIBROSIS QUISTICACLORUROGENESFil: Valdivieso, Ángel Gabriel. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; ArgentinaFil: Valdivieso, Ángel Gabriel. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Mori, Consuelo. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; ArgentinaFil: Mori, Consuelo. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Clauzure, Mariángeles. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; ArgentinaFil: Clauzure, Mariángeles. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Massip Copiz, María Macarena. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; ArgentinaFil: Massip Copiz, María Macarena. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Santa Coloma, Tomás Antonio. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; ArgentinaFil: Santa Coloma, Tomás Antonio. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaAbstract: In Cystic Fibrosis (CF), the impairment of the CFTR channel activity leads to a variety of alterations, including differential gene expression. However, the CFTR signaling mechanisms remain unclear. Recently, culturing IB3-1 CF cells under different intracellular Clconcentrations ([Cl- ]i), we observed several Cl- -dependent genes and further characterized one of them as RPS27. Thus, we hypothesized that Cl- might act as a signaling effector for CFTR signaling. Here, to test this idea, we study RPS27 expression in T84 cells modulating the CFTR activity by using CFTR inhibitors. First, we observed that incubation of T84 cells with increasing concentrations of the CFTR inhibitors CFTR(inh)-172 or GlyH-101 determined a progressive increase in the relative [Cl- ]i (using the Cl- fluorescent probe SPQ). The [Cl- ]i rise was concomitant with a dose-dependent down-regulation of RPS27. These results imply that CFTR inhibition produce Cl- accumulation and that RPS27 expression can be modulated by CFTR inhibition. Therefore, Cl- behaves as a signaling effector for CFTR in the modulation of RPS27 expression. In addition, the IL-1β receptor antagonist IL1RN or the JNK inhibitor SP600125, both restored the down-regulation of RPS27 induced by CFTRinh-172, implying a role of autocrine IL-1β and JNK signaling downstream of Cl- in RPS27 modulation.Elsevier2017info:eu-repo/semantics/articleinfo:eu-repo/semantics/acceptedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfhttps://repositorio.uca.edu.ar/handle/123456789/145601096-0384 (online)0003-986110.1016/j.abb.2017.09.01428941802Valdivieso, Á. et al. CFTR modulates RPS27 gene expression using chloride anion as signaling effector [en línea]. Postprint del artículo publicado en: Archives of Biochemistry and Biophysics. 2017 (633) . doi: https://doi.org/10.1016/j.abb.2017.09.014. Disponible en: https://repositorio.uca.edu.ar/handle/123456789/14560Archives of Biochemistry and Biophysics Vol. 633, 2017reponame:Repositorio Institucional (UCA)instname:Pontificia Universidad Católica Argentinaenginfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/4.0/2025-07-03T10:58:43Zoai:ucacris:123456789/14560instacron:UCAInstitucionalhttps://repositorio.uca.edu.ar/Universidad privadaNo correspondehttps://repositorio.uca.edu.ar/oaiclaudia_fernandez@uca.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:25852025-07-03 10:58:43.676Repositorio Institucional (UCA) - Pontificia Universidad Católica Argentinafalse
dc.title.none.fl_str_mv CFTR modulates RPS27 gene expression using chloride anion as signaling effector
title CFTR modulates RPS27 gene expression using chloride anion as signaling effector
spellingShingle CFTR modulates RPS27 gene expression using chloride anion as signaling effector
Valdivieso, Ángel Gabriel
REGULADOR DE CONDUCTANCIA DE TRANSMEMBRANA DE FIBROSIS QUISTICA
PROTEINA RIBOSOMICA 40S S27
FIBROSIS QUISTICA
CLORURO
GENES
title_short CFTR modulates RPS27 gene expression using chloride anion as signaling effector
title_full CFTR modulates RPS27 gene expression using chloride anion as signaling effector
title_fullStr CFTR modulates RPS27 gene expression using chloride anion as signaling effector
title_full_unstemmed CFTR modulates RPS27 gene expression using chloride anion as signaling effector
title_sort CFTR modulates RPS27 gene expression using chloride anion as signaling effector
dc.creator.none.fl_str_mv Valdivieso, Ángel Gabriel
Mori, Consuelo
Clauzure, Mariángeles
Massip Copiz, María Macarena
Santa Coloma, Tomás Antonio
author Valdivieso, Ángel Gabriel
author_facet Valdivieso, Ángel Gabriel
Mori, Consuelo
Clauzure, Mariángeles
Massip Copiz, María Macarena
Santa Coloma, Tomás Antonio
author_role author
author2 Mori, Consuelo
Clauzure, Mariángeles
Massip Copiz, María Macarena
Santa Coloma, Tomás Antonio
author2_role author
author
author
author
dc.subject.none.fl_str_mv REGULADOR DE CONDUCTANCIA DE TRANSMEMBRANA DE FIBROSIS QUISTICA
PROTEINA RIBOSOMICA 40S S27
FIBROSIS QUISTICA
CLORURO
GENES
topic REGULADOR DE CONDUCTANCIA DE TRANSMEMBRANA DE FIBROSIS QUISTICA
PROTEINA RIBOSOMICA 40S S27
FIBROSIS QUISTICA
CLORURO
GENES
dc.description.none.fl_txt_mv Fil: Valdivieso, Ángel Gabriel. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; Argentina
Fil: Valdivieso, Ángel Gabriel. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Mori, Consuelo. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; Argentina
Fil: Mori, Consuelo. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Clauzure, Mariángeles. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; Argentina
Fil: Clauzure, Mariángeles. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Massip Copiz, María Macarena. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; Argentina
Fil: Massip Copiz, María Macarena. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Santa Coloma, Tomás Antonio. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; Argentina
Fil: Santa Coloma, Tomás Antonio. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Abstract: In Cystic Fibrosis (CF), the impairment of the CFTR channel activity leads to a variety of alterations, including differential gene expression. However, the CFTR signaling mechanisms remain unclear. Recently, culturing IB3-1 CF cells under different intracellular Clconcentrations ([Cl- ]i), we observed several Cl- -dependent genes and further characterized one of them as RPS27. Thus, we hypothesized that Cl- might act as a signaling effector for CFTR signaling. Here, to test this idea, we study RPS27 expression in T84 cells modulating the CFTR activity by using CFTR inhibitors. First, we observed that incubation of T84 cells with increasing concentrations of the CFTR inhibitors CFTR(inh)-172 or GlyH-101 determined a progressive increase in the relative [Cl- ]i (using the Cl- fluorescent probe SPQ). The [Cl- ]i rise was concomitant with a dose-dependent down-regulation of RPS27. These results imply that CFTR inhibition produce Cl- accumulation and that RPS27 expression can be modulated by CFTR inhibition. Therefore, Cl- behaves as a signaling effector for CFTR in the modulation of RPS27 expression. In addition, the IL-1β receptor antagonist IL1RN or the JNK inhibitor SP600125, both restored the down-regulation of RPS27 induced by CFTRinh-172, implying a role of autocrine IL-1β and JNK signaling downstream of Cl- in RPS27 modulation.
description Fil: Valdivieso, Ángel Gabriel. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; Argentina
publishDate 2017
dc.date.none.fl_str_mv 2017
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/acceptedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str acceptedVersion
dc.identifier.none.fl_str_mv https://repositorio.uca.edu.ar/handle/123456789/14560
1096-0384 (online)
0003-9861
10.1016/j.abb.2017.09.014
28941802
Valdivieso, Á. et al. CFTR modulates RPS27 gene expression using chloride anion as signaling effector [en línea]. Postprint del artículo publicado en: Archives of Biochemistry and Biophysics. 2017 (633) . doi: https://doi.org/10.1016/j.abb.2017.09.014. Disponible en: https://repositorio.uca.edu.ar/handle/123456789/14560
url https://repositorio.uca.edu.ar/handle/123456789/14560
identifier_str_mv 1096-0384 (online)
0003-9861
10.1016/j.abb.2017.09.014
28941802
Valdivieso, Á. et al. CFTR modulates RPS27 gene expression using chloride anion as signaling effector [en línea]. Postprint del artículo publicado en: Archives of Biochemistry and Biophysics. 2017 (633) . doi: https://doi.org/10.1016/j.abb.2017.09.014. Disponible en: https://repositorio.uca.edu.ar/handle/123456789/14560
dc.language.none.fl_str_mv eng
language eng
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/4.0/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/4.0/
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Elsevier
publisher.none.fl_str_mv Elsevier
dc.source.none.fl_str_mv Archives of Biochemistry and Biophysics Vol. 633, 2017
reponame:Repositorio Institucional (UCA)
instname:Pontificia Universidad Católica Argentina
reponame_str Repositorio Institucional (UCA)
collection Repositorio Institucional (UCA)
instname_str Pontificia Universidad Católica Argentina
repository.name.fl_str_mv Repositorio Institucional (UCA) - Pontificia Universidad Católica Argentina
repository.mail.fl_str_mv claudia_fernandez@uca.edu.ar
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score 13.070432

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