Chloroquine normalizes aberrant transforming growth factor beta activity in cystic fibrosis bronchial epithelial cells
Identifieur interne : 001D62 ( Main/Exploration ); précédent : 001D61; suivant : 001D63Chloroquine normalizes aberrant transforming growth factor beta activity in cystic fibrosis bronchial epithelial cells
Auteurs : Elizabeth A. Perkett [États-Unis] ; Wojciech Ornatowski [États-Unis] ; Jens F. Poschet [États-Unis] ; Vojo Deretic [États-Unis]Source :
- Pediatric Pulmonology [ 8755-6863 ] ; 2006-08.
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.
- Pascal (Inist)
- MESH :
- Wicri :
- topic : Pédiatrie.
English descriptors
- KwdEn :
- Activity, Anomaly, Anti-Inflammatory Agents, Non-Steroidal (pharmacology), Antimalarial, Bronchi (cytology), Bronchus, Cells, Cultured, Chloroquine, Chloroquine (pharmacology), Chronic, Culture Media, Conditioned, Cystic Fibrosis (blood), Cystic Fibrosis (physiopathology), Cystic fibrosis, Epithelial Cells (metabolism), Epithelial cell, Fibrosis, Furin, Golgi apparatus, Humans, Inflammation, Lung, Lung (cytology), Parasiticide, Pediatrics, Respiratory disease, Transforming Growth Factor beta (blood), Transforming growth factor β, 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.
- Teeft :
- Assay, Beta, Biol, Breath condensate, Bronchial epithelial cells, Brosis, Cell line, Cell lines, Cell number, Cells, Cultured, Cftr, Cftr gene, Chloroquine, Chloroquine normalizes, Chloroquine treatment, Control cells, Control levels, Culture Media, Conditioned, Cystic, Cystic fibrosis foundation, Epithelial, Epithelial cell line, Epithelial cells, Extracellular, Extracellular microenvironment, Extracellular milieu, Furin, Grant sponsor, Growth factor beta, Humans, Individual isoforms, Luciferase, Luciferase activity, Luciferase assay, Lung development, Lung disease, Mexico health sciences center, Mlec, Mlec cells, More acidic, Normal cells, Open bars control cells, Pcep, Pediatr pulmonol, Perkett, Proc natl acad, Pulmonary hypertension, Respir, Respir cell, Responsive promoter, Rheumatoid arthritis, Separate experiments, Stable transfection, Tgfb activity, Total amount.
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‐β) 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‐β produced by CF and normal cells was measured using a reporter cell line with a TGF‐β 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‐β levels. Pediatr Pulmonol. 2006; 41: 771–778. © 2006 Wiley‐Liss, Inc.
Url:
DOI: 10.1002/ppul.20452
Affiliations:
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Le document en format XML
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épithéliales (métabolisme)</term><term>Chloroquine (pharmacologie)</term><term>Facteur de croissance transformant bêta (sang)</term><term>Humains</term><term>Milieux de culture conditionnés</term><term>Mucoviscidose (physiopathologie)</term><term>Mucoviscidose (sang)</term><term>Poumon (cytologie)</term><term>Réseau trans-golgien (métabolisme)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Transforming Growth Factor beta</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Anti-Inflammatory Agents, Non-Steroidal</term><term>Chloroquine</term></keywords><keywords scheme="MESH" qualifier="blood" xml:lang="en"><term>Cystic Fibrosis</term></keywords><keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Bronches</term><term>Poumon</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Bronchi</term><term>Lung</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Epithelial Cells</term><term>trans-Golgi Network</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cellules épithéliales</term><term>Réseau trans-golgien</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Anti-inflammatoires non stéroïdiens</term><term>Chloroquine</term></keywords><keywords scheme="MESH" qualifier="physiopathologie" xml:lang="fr"><term>Mucoviscidose</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Cystic Fibrosis</term></keywords><keywords scheme="MESH" qualifier="sang" xml:lang="fr"><term>Facteur de croissance transformant bêta</term><term>Mucoviscidose</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Activité</term><term>Anomalie</term><term>Antipaludique</term><term>Antiparasitaire</term><term>Appareil Golgi</term><term>Appareil respiratoire pathologie</term><term>Bronche</term><term>Cellule 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xml:lang="fr"><term>Pédiatrie</term></keywords></textClass></profileDesc></teiHeader><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‐β) 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‐β produced by CF and normal cells was measured using a reporter cell line with a TGF‐β 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‐β levels. Pediatr Pulmonol. 2006; 41: 771–778. © 2006 Wiley‐Liss, Inc.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Nouveau-Mexique</li></region></list><tree><country name="États-Unis"><region name="Nouveau-Mexique"><name sortKey="Perkett, Elizabeth A" sort="Perkett, Elizabeth A" uniqKey="Perkett E" first="Elizabeth A." last="Perkett">Elizabeth A. Perkett</name></region><name sortKey="Deretic, Vojo" sort="Deretic, Vojo" uniqKey="Deretic V" first="Vojo" last="Deretic">Vojo Deretic</name><name sortKey="Deretic, Vojo" sort="Deretic, Vojo" uniqKey="Deretic V" first="Vojo" last="Deretic">Vojo Deretic</name><name sortKey="Ornatowski, Wojciech" sort="Ornatowski, Wojciech" uniqKey="Ornatowski W" first="Wojciech" last="Ornatowski">Wojciech Ornatowski</name><name sortKey="Perkett, Elizabeth A" sort="Perkett, Elizabeth A" uniqKey="Perkett E" first="Elizabeth A." last="Perkett">Elizabeth A. Perkett</name><name sortKey="Perkett, Elizabeth A" sort="Perkett, Elizabeth A" uniqKey="Perkett E" first="Elizabeth A." last="Perkett">Elizabeth A. Perkett</name><name sortKey="Perkett, Elizabeth A" sort="Perkett, Elizabeth A" uniqKey="Perkett E" first="Elizabeth A." last="Perkett">Elizabeth A. Perkett</name><name sortKey="Poschet, Jens F" sort="Poschet, Jens F" uniqKey="Poschet J" first="Jens F." last="Poschet">Jens F. Poschet</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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