Chloroquine normalizes aberrant transforming growth factor beta activity in cystic fibrosis bronchial epithelial cells
Identifieur interne : 001E12 ( Main/Merge ); précédent : 001E11; suivant : 001E13Chloroquine normalizes aberrant transforming growth factor beta activity in cystic fibrosis bronchial epithelial cells
Auteurs : Elizabeth A. Perkett [États-Unis] ; Wojclech Ornatowski [États-Unis] ; Jens F. Poschet [États-Unis] ; Vojo Deretic [États-Unis]Source :
- Pediatric pulmonology [ 8755-6863 ] ; 2006.
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- Pascal (Inist)
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- topic : Pédiatrie.
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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-p) 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-p produced by CF and normal cells was measured using a reporter cell line with a TGF-p responsive promoter linked to luciferase. Increased levels of TGF-β 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-β were normalized with chloroquine indicating that the hyperacidification of the TGN of CF cells is responsible for the altered TGF-p levels.
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<series><title level="j" type="main">Pediatric pulmonology</title>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Activity</term>
<term>Anomaly</term>
<term>Antimalarial</term>
<term>Bronchus</term>
<term>Chloroquine</term>
<term>Chronic</term>
<term>Cystic fibrosis</term>
<term>Epithelial cell</term>
<term>Fibrosis</term>
<term>Furin</term>
<term>Golgi apparatus</term>
<term>Inflammation</term>
<term>Lung</term>
<term>Parasiticide</term>
<term>Pediatrics</term>
<term>Respiratory disease</term>
<term>Transforming growth factor β</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Mucoviscidose</term>
<term>Appareil respiratoire pathologie</term>
<term>Chloroquine</term>
<term>Anomalie</term>
<term>Facteur croissance transformant β</term>
<term>Activité</term>
<term>Bronche</term>
<term>Cellule épithéliale</term>
<term>Poumon</term>
<term>Fibrose</term>
<term>Chronique</term>
<term>Inflammation</term>
<term>Furin</term>
<term>Appareil Golgi</term>
<term>Pédiatrie</term>
<term>Antipaludique</term>
<term>Antiparasitaire</term>
</keywords>
<keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Pédiatrie</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-p) 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-p produced by CF and normal cells was measured using a reporter cell line with a TGF-p responsive promoter linked to luciferase. Increased levels of TGF-β 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-β were normalized with chloroquine indicating that the hyperacidification of the TGN of CF cells is responsible for the altered TGF-p levels.</div>
</front>
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<affiliations><list><country><li>États-Unis</li>
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<region><li>Nouveau-Mexique</li>
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<name sortKey="Deretic, Vojo" sort="Deretic, Vojo" uniqKey="Deretic V" first="Vojo" last="Deretic">Vojo Deretic</name>
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<name sortKey="Ornatowski, Wojclech" sort="Ornatowski, Wojclech" uniqKey="Ornatowski W" first="Wojclech" last="Ornatowski">Wojclech Ornatowski</name>
<name sortKey="Poschet, Jens F" sort="Poschet, Jens F" uniqKey="Poschet J" first="Jens F." last="Poschet">Jens F. Poschet</name>
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