Disruption of interleukin-1 β autocrine signaling rescues complex I activity and improves ROS levels in immortalized epithelial cells with impaired cystic fibrosis transmembrane co...

Autores
Clauzure, Mariángeles; Valdivieso, Ángel Gabriel; Massip Copiz, María Macarena; Schulman, Gustavo; Teiber, María Luz; Santa Coloma, Tomás Antonio
Año de publicación
2014
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Fil: Clauzure, Mariángeles. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; Argentina
Fil: Valdivieso, Ángel Gabriel. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; 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: Schulman, Gustavo. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; Argentina
Fil: Teiber, María Luz. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; 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: Clauzure, Mariángeles. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Valdivieso, Ángel Gabriel. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Massip Copiz, María Macarena. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Schulman, Gustavo. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Teiber, María Luz. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Santa Coloma, Tomás Antonio. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Abstract: Patients with cystic fibrosis (CF) have elevated concentration of cytokines in sputum and a general inflammatory condition. In addition, CF cells in culture produce diverse cytokines in excess, including IL-1b. We have previously shown that IL-1b, at low doses (,30 pM), can stimulate the expression of CFTR in T84 colon carcinoma cells, through NF-kB signaling. However, at higher doses (.2.5 ng/ml, ,150 pM), IL-1b inhibit CFTR mRNA expression. On the other hand, by using differential display, we found two genes with reduced expression in CF cells, corresponding to the mitochondrial proteins CISD1 and MTND4. The last is a key subunit for the activity of mitochondrial Complex I (mCx-I); accordingly, we later found a reduced mCx-I activity in CF cells. Here we found that IB3-1 cells (CF cells), cultured in serum-free media, secrete 32365 pg/ml of IL- 1b in 24 h vs 12763 pg/ml for S9 cells (CFTR-corrected IB3-1 cells). Externally added IL-1b (5 ng/ml) reduces the mCx-I activity and increases the mitochondrial (MitoSOX probe) and cellular (DCFH-DA probe) ROS levels of S9 (CFTR-corrected IB3-1 CF cells) or Caco-2/pRSctrl cells (shRNA control cells) to values comparable to those of IB3-1 or Caco-2/pRS26 cells (shRNA specific for CFTR). Treatments of IB3-1 or Caco-2/pRS26 cells with either IL-1b blocking antibody, IL-1 receptor antagonist, IKK inhibitor III (NF-kB pathway) or SB203580 (p38 MAPK pathway), restored the mCx-I activity. In addition, in IB3-1 or Caco-2/pRS26 cells, IL-1b blocking antibody, IKK inhibitor III or SB203580 reduced the mitochondrial ROS levels by ,50% and the cellular ROS levels near to basal values. The AP-1 inhibitors U0126 (MEK1/2) or SP600125 (JNK1/2/3 inhibitor) had no effects. The results suggest that in these cells IL-1b, through an autocrine effect, acts as a bridge connecting the CFTR with the mCx-I activity and the ROS levels.
Fuente
PLoS ONE Vol. 9, N° 6, 2014
Materia
MEDICINA
PROTEINAS
CELULAS EPITELIALES
FIBROSIS QUISTICA
CFTR
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:123456789/8675
Acceder
id RIUCA_44c2fceff09c33f27e7f12f632f6f4df
oai_identifier_str oai:ucacris:123456789/8675
network_acronym_str RIUCA
repository_id_str 2585
network_name_str Repositorio Institucional (UCA)
spelling Disruption of interleukin-1 β autocrine signaling rescues complex I activity and improves ROS levels in immortalized epithelial cells with impaired cystic fibrosis transmembrane conductance regulator (CFTR) functionClauzure, MariángelesValdivieso, Ángel GabrielMassip Copiz, María MacarenaSchulman, GustavoTeiber, María LuzSanta Coloma, Tomás AntonioMEDICINAPROTEINASCELULAS EPITELIALESFIBROSIS QUISTICACFTRGENESFil: Clauzure, Mariángeles. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; ArgentinaFil: Valdivieso, Ángel Gabriel. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; ArgentinaFil: Massip Copiz, María Macarena. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; ArgentinaFil: Schulman, Gustavo. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; ArgentinaFil: Teiber, María Luz. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; ArgentinaFil: Santa Coloma, Tomás Antonio. 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: Valdivieso, Ángel Gabriel. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Massip Copiz, María Macarena. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Schulman, Gustavo. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Teiber, María Luz. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Santa Coloma, Tomás Antonio. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaAbstract: Patients with cystic fibrosis (CF) have elevated concentration of cytokines in sputum and a general inflammatory condition. In addition, CF cells in culture produce diverse cytokines in excess, including IL-1b. We have previously shown that IL-1b, at low doses (,30 pM), can stimulate the expression of CFTR in T84 colon carcinoma cells, through NF-kB signaling. However, at higher doses (.2.5 ng/ml, ,150 pM), IL-1b inhibit CFTR mRNA expression. On the other hand, by using differential display, we found two genes with reduced expression in CF cells, corresponding to the mitochondrial proteins CISD1 and MTND4. The last is a key subunit for the activity of mitochondrial Complex I (mCx-I); accordingly, we later found a reduced mCx-I activity in CF cells. Here we found that IB3-1 cells (CF cells), cultured in serum-free media, secrete 32365 pg/ml of IL- 1b in 24 h vs 12763 pg/ml for S9 cells (CFTR-corrected IB3-1 cells). Externally added IL-1b (5 ng/ml) reduces the mCx-I activity and increases the mitochondrial (MitoSOX probe) and cellular (DCFH-DA probe) ROS levels of S9 (CFTR-corrected IB3-1 CF cells) or Caco-2/pRSctrl cells (shRNA control cells) to values comparable to those of IB3-1 or Caco-2/pRS26 cells (shRNA specific for CFTR). Treatments of IB3-1 or Caco-2/pRS26 cells with either IL-1b blocking antibody, IL-1 receptor antagonist, IKK inhibitor III (NF-kB pathway) or SB203580 (p38 MAPK pathway), restored the mCx-I activity. In addition, in IB3-1 or Caco-2/pRS26 cells, IL-1b blocking antibody, IKK inhibitor III or SB203580 reduced the mitochondrial ROS levels by ,50% and the cellular ROS levels near to basal values. The AP-1 inhibitors U0126 (MEK1/2) or SP600125 (JNK1/2/3 inhibitor) had no effects. The results suggest that in these cells IL-1b, through an autocrine effect, acts as a bridge connecting the CFTR with the mCx-I activity and the ROS levels.Dominik Hartl, University of Tübingen, Germany2014info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfhttps://repositorio.uca.edu.ar/handle/123456789/86751932-6203 (electrónico)10.1371/journal.pone.0099257Clauzure M, Valdivieso AG, Massip Copiz MM, Schulman G, Teiber ML, et al. (2014) Disruption of Interleukin-1b Autocrine Signaling Rescues Complex I Activity and Improves ROS Levels in Immortalized Epithelial Cells with Impaired Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) Function. PLoS ONE 9(6): e99257. doi:10.1371/journal.pone.0099257. Disponible en: https://repositorio.uca.edu.ar/handle/123456789/8675PLoS ONE Vol. 9, N° 6, 2014reponame:Repositorio Institucional (UCA)instname:Pontificia Universidad Católica Argentinaenginfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/4.0/2025-07-03T10:56:52Zoai:ucacris:123456789/8675instacron:UCAInstitucionalhttps://repositorio.uca.edu.ar/Universidad privadaNo correspondehttps://repositorio.uca.edu.ar/oaiclaudia_fernandez@uca.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:25852025-07-03 10:56:52.64Repositorio Institucional (UCA) - Pontificia Universidad Católica Argentinafalse
dc.title.none.fl_str_mv Disruption of interleukin-1 β autocrine signaling rescues complex I activity and improves ROS levels in immortalized epithelial cells with impaired cystic fibrosis transmembrane conductance regulator (CFTR) function
title Disruption of interleukin-1 β autocrine signaling rescues complex I activity and improves ROS levels in immortalized epithelial cells with impaired cystic fibrosis transmembrane conductance regulator (CFTR) function
spellingShingle Disruption of interleukin-1 β autocrine signaling rescues complex I activity and improves ROS levels in immortalized epithelial cells with impaired cystic fibrosis transmembrane conductance regulator (CFTR) function
Clauzure, Mariángeles
MEDICINA
PROTEINAS
CELULAS EPITELIALES
FIBROSIS QUISTICA
CFTR
GENES
title_short Disruption of interleukin-1 β autocrine signaling rescues complex I activity and improves ROS levels in immortalized epithelial cells with impaired cystic fibrosis transmembrane conductance regulator (CFTR) function
title_full Disruption of interleukin-1 β autocrine signaling rescues complex I activity and improves ROS levels in immortalized epithelial cells with impaired cystic fibrosis transmembrane conductance regulator (CFTR) function
title_fullStr Disruption of interleukin-1 β autocrine signaling rescues complex I activity and improves ROS levels in immortalized epithelial cells with impaired cystic fibrosis transmembrane conductance regulator (CFTR) function
title_full_unstemmed Disruption of interleukin-1 β autocrine signaling rescues complex I activity and improves ROS levels in immortalized epithelial cells with impaired cystic fibrosis transmembrane conductance regulator (CFTR) function
title_sort Disruption of interleukin-1 β autocrine signaling rescues complex I activity and improves ROS levels in immortalized epithelial cells with impaired cystic fibrosis transmembrane conductance regulator (CFTR) function
dc.creator.none.fl_str_mv Clauzure, Mariángeles
Valdivieso, Ángel Gabriel
Massip Copiz, María Macarena
Schulman, Gustavo
Teiber, María Luz
Santa Coloma, Tomás Antonio
author Clauzure, Mariángeles
author_facet Clauzure, Mariángeles
Valdivieso, Ángel Gabriel
Massip Copiz, María Macarena
Schulman, Gustavo
Teiber, María Luz
Santa Coloma, Tomás Antonio
author_role author
author2 Valdivieso, Ángel Gabriel
Massip Copiz, María Macarena
Schulman, Gustavo
Teiber, María Luz
Santa Coloma, Tomás Antonio
author2_role author
author
author
author
author
dc.subject.none.fl_str_mv MEDICINA
PROTEINAS
CELULAS EPITELIALES
FIBROSIS QUISTICA
CFTR
GENES
topic MEDICINA
PROTEINAS
CELULAS EPITELIALES
FIBROSIS QUISTICA
CFTR
GENES
dc.description.none.fl_txt_mv Fil: Clauzure, Mariángeles. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; Argentina
Fil: Valdivieso, Ángel Gabriel. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; 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: Schulman, Gustavo. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; Argentina
Fil: Teiber, María Luz. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; 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: Clauzure, Mariángeles. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Valdivieso, Ángel Gabriel. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Massip Copiz, María Macarena. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Schulman, Gustavo. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Teiber, María Luz. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Santa Coloma, Tomás Antonio. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Abstract: Patients with cystic fibrosis (CF) have elevated concentration of cytokines in sputum and a general inflammatory condition. In addition, CF cells in culture produce diverse cytokines in excess, including IL-1b. We have previously shown that IL-1b, at low doses (,30 pM), can stimulate the expression of CFTR in T84 colon carcinoma cells, through NF-kB signaling. However, at higher doses (.2.5 ng/ml, ,150 pM), IL-1b inhibit CFTR mRNA expression. On the other hand, by using differential display, we found two genes with reduced expression in CF cells, corresponding to the mitochondrial proteins CISD1 and MTND4. The last is a key subunit for the activity of mitochondrial Complex I (mCx-I); accordingly, we later found a reduced mCx-I activity in CF cells. Here we found that IB3-1 cells (CF cells), cultured in serum-free media, secrete 32365 pg/ml of IL- 1b in 24 h vs 12763 pg/ml for S9 cells (CFTR-corrected IB3-1 cells). Externally added IL-1b (5 ng/ml) reduces the mCx-I activity and increases the mitochondrial (MitoSOX probe) and cellular (DCFH-DA probe) ROS levels of S9 (CFTR-corrected IB3-1 CF cells) or Caco-2/pRSctrl cells (shRNA control cells) to values comparable to those of IB3-1 or Caco-2/pRS26 cells (shRNA specific for CFTR). Treatments of IB3-1 or Caco-2/pRS26 cells with either IL-1b blocking antibody, IL-1 receptor antagonist, IKK inhibitor III (NF-kB pathway) or SB203580 (p38 MAPK pathway), restored the mCx-I activity. In addition, in IB3-1 or Caco-2/pRS26 cells, IL-1b blocking antibody, IKK inhibitor III or SB203580 reduced the mitochondrial ROS levels by ,50% and the cellular ROS levels near to basal values. The AP-1 inhibitors U0126 (MEK1/2) or SP600125 (JNK1/2/3 inhibitor) had no effects. The results suggest that in these cells IL-1b, through an autocrine effect, acts as a bridge connecting the CFTR with the mCx-I activity and the ROS levels.
description Fil: Clauzure, Mariángeles. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; Argentina
publishDate 2014
dc.date.none.fl_str_mv 2014
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 https://repositorio.uca.edu.ar/handle/123456789/8675
1932-6203 (electrónico)
10.1371/journal.pone.0099257
Clauzure M, Valdivieso AG, Massip Copiz MM, Schulman G, Teiber ML, et al. (2014) Disruption of Interleukin-1b Autocrine Signaling Rescues Complex I Activity and Improves ROS Levels in Immortalized Epithelial Cells with Impaired Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) Function. PLoS ONE 9(6): e99257. doi:10.1371/journal.pone.0099257. Disponible en: https://repositorio.uca.edu.ar/handle/123456789/8675
url https://repositorio.uca.edu.ar/handle/123456789/8675
identifier_str_mv 1932-6203 (electrónico)
10.1371/journal.pone.0099257
Clauzure M, Valdivieso AG, Massip Copiz MM, Schulman G, Teiber ML, et al. (2014) Disruption of Interleukin-1b Autocrine Signaling Rescues Complex I Activity and Improves ROS Levels in Immortalized Epithelial Cells with Impaired Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) Function. PLoS ONE 9(6): e99257. doi:10.1371/journal.pone.0099257. Disponible en: https://repositorio.uca.edu.ar/handle/123456789/8675
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 Dominik Hartl, University of Tübingen, Germany
publisher.none.fl_str_mv Dominik Hartl, University of Tübingen, Germany
dc.source.none.fl_str_mv PLoS ONE Vol. 9, N° 6, 2014
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 13.22299

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