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
- Institución
- Pontificia Universidad Católica Argentina
- OAI Identificador
- oai:ucacris:123456789/8675
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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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13.070432 |