Chloroquine normalizes aberrant transforming growth factor beta activity in cystic fibrosis bronchial epithelial cells.
Identifieur interne : 000434 ( PubMed/Curation ); précédent : 000433; suivant : 000435Chloroquine normalizes aberrant transforming growth factor beta activity in cystic fibrosis bronchial epithelial cells.
Auteurs : Elizabeth A. Perkett [États-Unis] ; Wojciech Ornatowski ; Jens F. Poschet ; Vojo DereticSource :
- Pediatric pulmonology [ 8755-6863 ] ; 2006.
Descripteurs français
- KwdFr :
- Anti-inflammatoires non stéroïdiens (pharmacologie), Bronches (cytologie), Cellules cultivées, Cellules épithéliales (métabolisme), Chloroquine (pharmacologie), Facteur de croissance transformant bêta (sang), Humains, Milieux de culture conditionnés, Mucoviscidose (physiopathologie), Mucoviscidose (sang), Poumon (cytologie), Réseau trans-golgien (métabolisme).
- MESH :
- cytologie : Bronches, Poumon.
- métabolisme : Cellules épithéliales, Réseau trans-golgien.
- pharmacologie : Anti-inflammatoires non stéroïdiens, Chloroquine.
- physiopathologie : Mucoviscidose.
- sang : Facteur de croissance transformant bêta, Mucoviscidose.
- Cellules cultivées, Humains, Milieux de culture conditionnés.
English descriptors
- KwdEn :
- Anti-Inflammatory Agents, Non-Steroidal (pharmacology), Bronchi (cytology), Cells, Cultured, Chloroquine (pharmacology), Culture Media, Conditioned, Cystic Fibrosis (blood), Cystic Fibrosis (physiopathology), Epithelial Cells (metabolism), Humans, Lung (cytology), Transforming Growth Factor beta (blood), trans-Golgi Network (metabolism).
- MESH :
- chemical , blood : Transforming Growth Factor beta.
- chemical , pharmacology : Anti-Inflammatory Agents, Non-Steroidal, Chloroquine.
- blood : Cystic Fibrosis.
- cytology : Bronchi, Lung.
- metabolism : Epithelial Cells, trans-Golgi Network.
- physiopathology : Cystic Fibrosis.
- Cells, Cultured, Culture Media, Conditioned, Humans.
Abstract
Cystic fibrosis (CF) remains a fatal progressive disease in spite of the discovery and characterization of the CFTR gene. Transforming growth factor beta (TGF-beta) has been implicated in pathophysiology of CF. Previous reports have shown the trans-Golgi network (TGN) is hyperacdified in CF epithelial cells in culture and that this hyperacidification can be corrected with the membrane permeant weak base, chloroquine. In this study bioactive TGF-beta produced by CF and normal cells was measured using a reporter cell line with a TGF-beta responsive promoter linked to luciferase. Increased levels of TGF-beta were detected in the conditioned media from CF epithelial cells compared to their matched controls-(IB3-1 vs. S9; pCEP-R vs. pCEP, CuFi-4 vs. NuLi-1). Levels of TGF-beta were normalized with chloroquine indicating that the hyperacidification of the TGN of CF cells is responsible for the altered TGF-beta levels.
DOI: 10.1002/ppul.20452
PubMed: 16779853
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pubmed:16779853Le document en format XML
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<term>Chloroquine (pharmacology)</term>
<term>Culture Media, Conditioned</term>
<term>Cystic Fibrosis (blood)</term>
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<term>Epithelial Cells (metabolism)</term>
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<term>trans-Golgi Network (metabolism)</term>
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<term>Cellules cultivées</term>
<term>Cellules épithéliales (métabolisme)</term>
<term>Chloroquine (pharmacologie)</term>
<term>Facteur de croissance transformant bêta (sang)</term>
<term>Humains</term>
<term>Milieux de culture conditionnés</term>
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<term>Chloroquine</term>
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<keywords scheme="MESH" qualifier="blood" xml:lang="en"><term>Cystic Fibrosis</term>
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<keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Bronches</term>
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<term>Mucoviscidose</term>
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<term>Culture Media, Conditioned</term>
<term>Humans</term>
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<front><div type="abstract" xml:lang="en">Cystic fibrosis (CF) remains a fatal progressive disease in spite of the discovery and characterization of the CFTR gene. Transforming growth factor beta (TGF-beta) has been implicated in pathophysiology of CF. Previous reports have shown the trans-Golgi network (TGN) is hyperacdified in CF epithelial cells in culture and that this hyperacidification can be corrected with the membrane permeant weak base, chloroquine. In this study bioactive TGF-beta produced by CF and normal cells was measured using a reporter cell line with a TGF-beta responsive promoter linked to luciferase. Increased levels of TGF-beta were detected in the conditioned media from CF epithelial cells compared to their matched controls-(IB3-1 vs. S9; pCEP-R vs. pCEP, CuFi-4 vs. NuLi-1). Levels of TGF-beta were normalized with chloroquine indicating that the hyperacidification of the TGN of CF cells is responsible for the altered TGF-beta levels.</div>
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<Abstract><AbstractText>Cystic fibrosis (CF) remains a fatal progressive disease in spite of the discovery and characterization of the CFTR gene. Transforming growth factor beta (TGF-beta) has been implicated in pathophysiology of CF. Previous reports have shown the trans-Golgi network (TGN) is hyperacdified in CF epithelial cells in culture and that this hyperacidification can be corrected with the membrane permeant weak base, chloroquine. In this study bioactive TGF-beta produced by CF and normal cells was measured using a reporter cell line with a TGF-beta responsive promoter linked to luciferase. Increased levels of TGF-beta were detected in the conditioned media from CF epithelial cells compared to their matched controls-(IB3-1 vs. S9; pCEP-R vs. pCEP, CuFi-4 vs. NuLi-1). Levels of TGF-beta were normalized with chloroquine indicating that the hyperacidification of the TGN of CF cells is responsible for the altered TGF-beta levels.</AbstractText>
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