ChloroquineV1, PubMed, Corpus, bibRecord, 000434

Chloroquine normalizes aberrant transforming growth factor beta activity in cystic fibrosis bronchial epithelial cells.

Identifieur interne : 000434 ( PubMed/Corpus ); précédent : 000433; suivant : 000435

Chloroquine normalizes aberrant transforming growth factor beta activity in cystic fibrosis bronchial epithelial cells.

Auteurs : Elizabeth A. Perkett ; Wojciech Ornatowski ; Jens F. Poschet ; Vojo Deretic

Source :

Pediatric pulmonology [ 8755-6863 ] ; 2006.

RBID : pubmed:16779853

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

Links to Exploration step

pubmed:16779853

Le document en format XML

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<author><name sortKey="Perkett, Elizabeth A" sort="Perkett, Elizabeth A" uniqKey="Perkett E" first="Elizabeth A" last="Perkett">Elizabeth A. Perkett</name>
<affiliation><nlm:affiliation>Department of Pediatrics, University of New Mexico Health Sciences Center, Albuquerque, New Mexico 87131-0001, USA. eperkett@salud.unm.edu</nlm:affiliation>
</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>
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<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><nlm:affiliation>Department of Pediatrics, University of New Mexico Health Sciences Center, Albuquerque, New Mexico 87131-0001, USA. eperkett@salud.unm.edu</nlm:affiliation>
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<author><name sortKey="Ornatowski, Wojciech" sort="Ornatowski, Wojciech" uniqKey="Ornatowski W" first="Wojciech" last="Ornatowski">Wojciech Ornatowski</name>
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<author><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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<author><name sortKey="Deretic, Vojo" sort="Deretic, Vojo" uniqKey="Deretic V" first="Vojo" last="Deretic">Vojo Deretic</name>
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<series><title level="j">Pediatric pulmonology</title>
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<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="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>
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<keywords scheme="MESH" qualifier="blood" xml:lang="en"><term>Cystic Fibrosis</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="physiopathology" xml:lang="en"><term>Cystic Fibrosis</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Cells, Cultured</term>
<term>Culture Media, Conditioned</term>
<term>Humans</term>
</keywords>
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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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<Month>12</Month>
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<DateRevised><Year>2013</Year>
<Month>11</Month>
<Day>21</Day>
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<Article PubModel="Print"><Journal><ISSN IssnType="Print">8755-6863</ISSN>
<JournalIssue CitedMedium="Print"><Volume>41</Volume>
<Issue>8</Issue>
<PubDate><Year>2006</Year>
<Month>Aug</Month>
</PubDate>
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<Title>Pediatric pulmonology</Title>
<ISOAbbreviation>Pediatr. Pulmonol.</ISOAbbreviation>
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<ArticleTitle>Chloroquine normalizes aberrant transforming growth factor beta activity in cystic fibrosis bronchial epithelial cells.</ArticleTitle>
<Pagination><MedlinePgn>771-8</MedlinePgn>
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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>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Perkett</LastName>
<ForeName>Elizabeth A</ForeName>
<Initials>EA</Initials>
<AffiliationInfo><Affiliation>Department of Pediatrics, University of New Mexico Health Sciences Center, Albuquerque, New Mexico 87131-0001, USA. eperkett@salud.unm.edu</Affiliation>
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<Author ValidYN="Y"><LastName>Poschet</LastName>
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<Author ValidYN="Y"><LastName>Deretic</LastName>
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<Language>eng</Language>
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<Acronym>AI</Acronym>
<Agency>NIAID NIH HHS</Agency>
<Country>United States</Country>
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<MeshHeading><DescriptorName UI="D017077" MajorTopicYN="N">Culture Media, Conditioned</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D003550" MajorTopicYN="N">Cystic Fibrosis</DescriptorName>
<QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName>
<QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004847" MajorTopicYN="N">Epithelial Cells</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008168" MajorTopicYN="N">Lung</DescriptorName>
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</MeshHeading>
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Chloroquine normalizes aberrant transforming growth factor beta activity in cystic fibrosis bronchial epithelial cells.

Chloroquine normalizes aberrant transforming growth factor beta activity in cystic fibrosis bronchial epithelial cells.

Source :

English descriptors

Abstract

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