Chloroquine normalizes aberrant transforming growth factor beta activity in cystic fibrosis bronchial epithelial cells
Identifieur interne : 001D74 ( Main/Merge ); précédent : 001D73; suivant : 001D75Chloroquine 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.
- 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.
- 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
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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="Teeft" xml:lang="en"><term>Assay</term><term>Beta</term><term>Biol</term><term>Breath condensate</term><term>Bronchial epithelial cells</term><term>Brosis</term><term>Cell line</term><term>Cell lines</term><term>Cell number</term><term>Cells, Cultured</term><term>Cftr</term><term>Cftr gene</term><term>Chloroquine</term><term>Chloroquine normalizes</term><term>Chloroquine treatment</term><term>Control cells</term><term>Control levels</term><term>Culture Media, Conditioned</term><term>Cystic</term><term>Cystic fibrosis foundation</term><term>Epithelial</term><term>Epithelial cell line</term><term>Epithelial cells</term><term>Extracellular</term><term>Extracellular microenvironment</term><term>Extracellular milieu</term><term>Furin</term><term>Grant sponsor</term><term>Growth factor beta</term><term>Humans</term><term>Individual isoforms</term><term>Luciferase</term><term>Luciferase activity</term><term>Luciferase assay</term><term>Lung development</term><term>Lung disease</term><term>Mexico health sciences center</term><term>Mlec</term><term>Mlec cells</term><term>More acidic</term><term>Normal cells</term><term>Open bars control cells</term><term>Pcep</term><term>Pediatr pulmonol</term><term>Perkett</term><term>Proc natl acad</term><term>Pulmonary hypertension</term><term>Respir</term><term>Respir cell</term><term>Responsive promoter</term><term>Rheumatoid arthritis</term><term>Separate experiments</term><term>Stable transfection</term><term>Tgfb activity</term><term>Total amount</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Cellules cultivées</term><term>Humains</term><term>Milieux de culture conditionnés</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><double doi="10.1002/ppul.20452"><ISTEX><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Chloroquine normalizes aberrant transforming growth factor beta activity in cystic fibrosis bronchial epithelial cells</title><author><name sortKey="Perkett, Elizabeth A" sort="Perkett, Elizabeth A" uniqKey="Perkett E" first="Elizabeth A." last="Perkett">Elizabeth A. Perkett</name></author><author><name sortKey="Ornatowski, Wojciech" sort="Ornatowski, Wojciech" uniqKey="Ornatowski W" first="Wojciech" last="Ornatowski">Wojciech Ornatowski</name></author><author><name sortKey="Poschet, Jens F" sort="Poschet, Jens F" uniqKey="Poschet J" first="Jens F." last="Poschet">Jens F. Poschet</name></author><author><name sortKey="Deretic, Vojo" sort="Deretic, Vojo" uniqKey="Deretic V" first="Vojo" last="Deretic">Vojo Deretic</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:A2849A46DE7DDD029AF6A556308714E9B3453E4A</idno><date when="2006" year="2006">2006</date><idno type="doi">10.1002/ppul.20452</idno><idno type="url">https://api.istex.fr/ark:/67375/WNG-S3CWTFMW-C/fulltext.pdf</idno><idno type="wicri:Area/Istex/Corpus">000060</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">000060</idno><idno type="wicri:Area/Istex/Curation">000060</idno><idno type="wicri:Area/Istex/Checkpoint">000C30</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Checkpoint">000C30</idno><idno type="wicri:doubleKey">8755-6863:2006:Perkett E:chloroquine:normalizes:aberrant</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main">Chloroquine normalizes aberrant transforming growth factor beta activity in cystic fibrosis bronchial epithelial cells</title><author><name sortKey="Perkett, Elizabeth A" sort="Perkett, Elizabeth A" uniqKey="Perkett E" first="Elizabeth A." last="Perkett">Elizabeth A. Perkett</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Nouveau-Mexique</region></placeName><wicri:cityArea>Department of Pediatrics, University of New Mexico Health Sciences Center, Albuquerque</wicri:cityArea></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Nouveau-Mexique</region></placeName><wicri:cityArea>Department of Cell Biology and Physiology, University of New Mexico Health Sciences Center, Albuquerque</wicri:cityArea></affiliation><affiliation wicri:level="1"><country wicri:rule="url">États-Unis</country></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Nouveau-Mexique</region></placeName><wicri:cityArea>Correspondence address: Pediatrics Pulmonary, MSC 10‐5590, 1 University of New Mexico, Albuquerque</wicri:cityArea></affiliation></author><author><name sortKey="Ornatowski, Wojciech" sort="Ornatowski, Wojciech" uniqKey="Ornatowski W" first="Wojciech" last="Ornatowski">Wojciech Ornatowski</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Nouveau-Mexique</region></placeName><wicri:cityArea>Department of Molecular Genetics and Microbiology, University of New Mexico Health Sciences Center, Albuquerque</wicri:cityArea></affiliation></author><author><name sortKey="Poschet, Jens F" sort="Poschet, Jens F" uniqKey="Poschet J" first="Jens F." last="Poschet">Jens F. Poschet</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Nouveau-Mexique</region></placeName><wicri:cityArea>Department of Molecular Genetics and Microbiology, University of New Mexico Health Sciences Center, Albuquerque</wicri:cityArea></affiliation></author><author><name sortKey="Deretic, Vojo" sort="Deretic, Vojo" uniqKey="Deretic V" first="Vojo" last="Deretic">Vojo Deretic</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Nouveau-Mexique</region></placeName><wicri:cityArea>Department of Cell Biology and Physiology, University of New Mexico Health Sciences Center, Albuquerque</wicri:cityArea></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Nouveau-Mexique</region></placeName><wicri:cityArea>Department of Molecular Genetics and Microbiology, University of New Mexico Health Sciences Center, Albuquerque</wicri:cityArea></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Pediatric Pulmonology</title><title level="j" type="alt">PEDIATRIC PULMONOLOGY</title><idno type="ISSN">8755-6863</idno><idno type="eISSN">1099-0496</idno><imprint><biblScope unit="vol">41</biblScope><biblScope unit="issue">8</biblScope><biblScope unit="page" from="771">771</biblScope><biblScope unit="page" to="778">778</biblScope><biblScope unit="page-count">8</biblScope><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2006-08">2006-08</date></imprint><idno type="ISSN">8755-6863</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">8755-6863</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Assay</term><term>Beta</term><term>Biol</term><term>Breath condensate</term><term>Bronchial epithelial cells</term><term>Brosis</term><term>Cell line</term><term>Cell lines</term><term>Cell number</term><term>Cftr</term><term>Cftr gene</term><term>Chloroquine</term><term>Chloroquine normalizes</term><term>Chloroquine treatment</term><term>Control cells</term><term>Control levels</term><term>Cystic</term><term>Cystic fibrosis foundation</term><term>Epithelial</term><term>Epithelial cell line</term><term>Epithelial cells</term><term>Extracellular</term><term>Extracellular microenvironment</term><term>Extracellular milieu</term><term>Furin</term><term>Grant sponsor</term><term>Growth factor beta</term><term>Individual isoforms</term><term>Luciferase</term><term>Luciferase activity</term><term>Luciferase assay</term><term>Lung development</term><term>Lung disease</term><term>Mexico health sciences center</term><term>Mlec</term><term>Mlec cells</term><term>More acidic</term><term>Normal cells</term><term>Open bars control cells</term><term>Pcep</term><term>Pediatr pulmonol</term><term>Perkett</term><term>Proc natl acad</term><term>Pulmonary hypertension</term><term>Respir</term><term>Respir cell</term><term>Responsive promoter</term><term>Rheumatoid arthritis</term><term>Separate experiments</term><term>Stable transfection</term><term>Tgfb activity</term><term>Total amount</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></ISTEX><PubMed><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Chloroquine normalizes aberrant transforming growth factor beta activity in cystic fibrosis bronchial epithelial cells.</title><author><name sortKey="Perkett, Elizabeth A" sort="Perkett, Elizabeth A" uniqKey="Perkett E" first="Elizabeth A" last="Perkett">Elizabeth A. Perkett</name><affiliation wicri:level="1"><nlm:affiliation>Department of Pediatrics, University of New Mexico Health Sciences Center, Albuquerque, New Mexico 87131-0001, USA. eperkett@salud.unm.edu</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pediatrics, University of New Mexico Health Sciences Center, Albuquerque, New Mexico 87131-0001</wicri:regionArea><wicri:noRegion>New Mexico 87131-0001</wicri:noRegion></affiliation></author><author><name sortKey="Ornatowski, Wojciech" sort="Ornatowski, Wojciech" uniqKey="Ornatowski W" first="Wojciech" last="Ornatowski">Wojciech Ornatowski</name></author><author><name sortKey="Poschet, Jens F" sort="Poschet, Jens F" uniqKey="Poschet J" first="Jens F" last="Poschet">Jens F. Poschet</name></author><author><name sortKey="Deretic, Vojo" sort="Deretic, Vojo" uniqKey="Deretic V" first="Vojo" last="Deretic">Vojo Deretic</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2006">2006</date><idno type="RBID">pubmed:16779853</idno><idno type="pmid">16779853</idno><idno type="doi">10.1002/ppul.20452</idno><idno type="wicri:Area/PubMed/Corpus">000434</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000434</idno><idno type="wicri:Area/PubMed/Curation">000434</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000434</idno><idno type="wicri:Area/PubMed/Checkpoint">000421</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">000421</idno><idno type="wicri:Area/Ncbi/Merge">000089</idno><idno type="wicri:Area/Ncbi/Curation">000089</idno><idno type="wicri:Area/Ncbi/Checkpoint">000089</idno><idno type="wicri:doubleKey">8755-6863:2006:Perkett E:chloroquine:normalizes:aberrant</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Chloroquine normalizes aberrant transforming growth factor beta activity in cystic fibrosis bronchial epithelial cells.</title><author><name sortKey="Perkett, Elizabeth A" sort="Perkett, Elizabeth A" uniqKey="Perkett E" first="Elizabeth A" last="Perkett">Elizabeth A. Perkett</name><affiliation wicri:level="1"><nlm:affiliation>Department of Pediatrics, University of New Mexico Health Sciences Center, Albuquerque, New Mexico 87131-0001, USA. eperkett@salud.unm.edu</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pediatrics, University of New Mexico Health Sciences Center, Albuquerque, New Mexico 87131-0001</wicri:regionArea><wicri:noRegion>New Mexico 87131-0001</wicri:noRegion></affiliation></author><author><name sortKey="Ornatowski, Wojciech" sort="Ornatowski, Wojciech" uniqKey="Ornatowski W" first="Wojciech" last="Ornatowski">Wojciech Ornatowski</name></author><author><name sortKey="Poschet, Jens F" sort="Poschet, Jens F" uniqKey="Poschet J" first="Jens F" last="Poschet">Jens F. Poschet</name></author><author><name sortKey="Deretic, Vojo" sort="Deretic, Vojo" uniqKey="Deretic V" first="Vojo" last="Deretic">Vojo Deretic</name></author></analytic><series><title level="j">Pediatric pulmonology</title><idno type="ISSN">8755-6863</idno><imprint><date when="2006" type="published">2006</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Anti-Inflammatory Agents, Non-Steroidal (pharmacology)</term><term>Bronchi (cytology)</term><term>Cells, Cultured</term><term>Chloroquine (pharmacology)</term><term>Culture Media, Conditioned</term><term>Cystic Fibrosis (blood)</term><term>Cystic Fibrosis (physiopathology)</term><term>Epithelial Cells (metabolism)</term><term>Humans</term><term>Lung (cytology)</term><term>Transforming Growth Factor beta (blood)</term><term>trans-Golgi Network (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Anti-inflammatoires non stéroïdiens (pharmacologie)</term><term>Bronches (cytologie)</term><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><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="MESH" xml:lang="en"><term>Cells, Cultured</term><term>Culture Media, Conditioned</term><term>Humans</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Cellules cultivées</term><term>Humains</term><term>Milieux de culture conditionnés</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-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></front></TEI></PubMed></double></record>Pour manipuler ce document sous Unix (Dilib)
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