File Download
 
Links for fulltext
(May Require Subscription)
 
Supplementary

Article: Nonsteroidal anti-inflammatory drugs upregulate function of wild-type and mutant CFTR
  • Basic View
  • Metadata View
  • XML View
TitleNonsteroidal anti-inflammatory drugs upregulate function of wild-type and mutant CFTR
 
AuthorsLi, J3
Xiang, YY3
Ye, L4
Tsui, LC2 4
MacDonald, JF1
Hu, J4 3
Lu, WY5 3 1
 
KeywordsAdenylate cyclase
Chloride channel
Forskolin
Lung epithelium
Perforated-patch recording
 
Issue Date2008
 
PublisherEuropean Respiratory Society. The Journal's web site is located at http://erj.ersjournals.com
 
CitationEuropean Respiratory Journal, 2008, v. 32 n. 2, p. 334-343 [How to Cite?]
DOI: http://dx.doi.org/10.1183/09031936.00168007
 
AbstractSmall-scale clinical trials show that treatment of cystic fibrosis (CF) patients with ibuprofen, a nonsteroidal anti-inflammatory drug, improves the symptoms of CF and slows down the decline of lung function. Paradoxically, ibuprofen inhibits ligand-stimulated CF transmembrance conductance regulator (CFTR) activity. The aim of the present study was to investigate the effects of ibuprofen on CFTR function under different conditions. Patch-clamp recordings were performed in two lines of human airway epithelial cells: IB3-8-3-7 cells, which express wild-type CFTR; and IB3-1 cells, which express the variant CFTR with deletion of phenylalanine 580 (ΔF580CFTR). Addition of ibuprofen to the extracellular solution caused a rapid inhibition of CFTR activity in IB3-8-3-7 cells in the presence of a high intracellular concentration of cAMP, whereas ibuprofen enhanced the CFTR conductance at low levels of cAMP. Introducing ibuprofen into the interior of cells occluded the enhancing effect of ibuprofen. Notably, the variant CFTR-mediated conductance was detected in IB3-1 cells treated with myoinositol and was enhanced by ibuprofen at endogenous levels of cAMP. In summary, nonsteroidal anti-inflammatory drugs increase the function of both wild-type cystic fibrosis transmembrane conductance regulator and the phenylalanine 580 deletion in cultured human airway epithelial cells at endogenous levels of cAMP. Copyright©ERS Journals Ltd 2008.
 
ISSN0903-1936
2012 Impact Factor: 6.355
2012 SCImago Journal Rankings: 2.433
 
DOIhttp://dx.doi.org/10.1183/09031936.00168007
 
ISI Accession Number IDWOS:000258417000014
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorLi, J
 
dc.contributor.authorXiang, YY
 
dc.contributor.authorYe, L
 
dc.contributor.authorTsui, LC
 
dc.contributor.authorMacDonald, JF
 
dc.contributor.authorHu, J
 
dc.contributor.authorLu, WY
 
dc.date.accessioned2011-11-25T08:30:12Z
 
dc.date.available2011-11-25T08:30:12Z
 
dc.date.issued2008
 
dc.description.abstractSmall-scale clinical trials show that treatment of cystic fibrosis (CF) patients with ibuprofen, a nonsteroidal anti-inflammatory drug, improves the symptoms of CF and slows down the decline of lung function. Paradoxically, ibuprofen inhibits ligand-stimulated CF transmembrance conductance regulator (CFTR) activity. The aim of the present study was to investigate the effects of ibuprofen on CFTR function under different conditions. Patch-clamp recordings were performed in two lines of human airway epithelial cells: IB3-8-3-7 cells, which express wild-type CFTR; and IB3-1 cells, which express the variant CFTR with deletion of phenylalanine 580 (ΔF580CFTR). Addition of ibuprofen to the extracellular solution caused a rapid inhibition of CFTR activity in IB3-8-3-7 cells in the presence of a high intracellular concentration of cAMP, whereas ibuprofen enhanced the CFTR conductance at low levels of cAMP. Introducing ibuprofen into the interior of cells occluded the enhancing effect of ibuprofen. Notably, the variant CFTR-mediated conductance was detected in IB3-1 cells treated with myoinositol and was enhanced by ibuprofen at endogenous levels of cAMP. In summary, nonsteroidal anti-inflammatory drugs increase the function of both wild-type cystic fibrosis transmembrane conductance regulator and the phenylalanine 580 deletion in cultured human airway epithelial cells at endogenous levels of cAMP. Copyright©ERS Journals Ltd 2008.
 
dc.description.naturelink_to_OA_fulltext
 
dc.identifier.citationEuropean Respiratory Journal, 2008, v. 32 n. 2, p. 334-343 [How to Cite?]
DOI: http://dx.doi.org/10.1183/09031936.00168007
 
dc.identifier.doihttp://dx.doi.org/10.1183/09031936.00168007
 
dc.identifier.epage343
 
dc.identifier.isiWOS:000258417000014
 
dc.identifier.issn0903-1936
2012 Impact Factor: 6.355
2012 SCImago Journal Rankings: 2.433
 
dc.identifier.issue2
 
dc.identifier.openurl
 
dc.identifier.pmid18385167
 
dc.identifier.scopuseid_2-s2.0-55149090254
 
dc.identifier.spage334
 
dc.identifier.urihttp://hdl.handle.net/10722/143454
 
dc.identifier.volume32
 
dc.languageeng
 
dc.publisherEuropean Respiratory Society. The Journal's web site is located at http://erj.ersjournals.com
 
dc.publisher.placeSwitzerland
 
dc.relation.ispartofEuropean Respiratory Journal
 
dc.relation.referencesReferences in Scopus
 
dc.subject.meshAnti-Inflammatory Agents, Non-Steroidal - pharmacology
 
dc.subject.meshCystic Fibrosis - metabolism
 
dc.subject.meshCystic Fibrosis Transmembrane Conductance Regulator - genetics - metabolism
 
dc.subject.meshLung - drug effects - microbiology - pathology
 
dc.subject.meshMutation
 
dc.subjectAdenylate cyclase
 
dc.subjectChloride channel
 
dc.subjectForskolin
 
dc.subjectLung epithelium
 
dc.subjectPerforated-patch recording
 
dc.titleNonsteroidal anti-inflammatory drugs upregulate function of wild-type and mutant CFTR
 
dc.typeArticle
 
<?xml encoding="utf-8" version="1.0"?>
<item><contributor.author>Li, J</contributor.author>
<contributor.author>Xiang, YY</contributor.author>
<contributor.author>Ye, L</contributor.author>
<contributor.author>Tsui, LC</contributor.author>
<contributor.author>MacDonald, JF</contributor.author>
<contributor.author>Hu, J</contributor.author>
<contributor.author>Lu, WY</contributor.author>
<date.accessioned>2011-11-25T08:30:12Z</date.accessioned>
<date.available>2011-11-25T08:30:12Z</date.available>
<date.issued>2008</date.issued>
<identifier.citation>European Respiratory Journal, 2008, v. 32 n. 2, p. 334-343</identifier.citation>
<identifier.issn>0903-1936</identifier.issn>
<identifier.uri>http://hdl.handle.net/10722/143454</identifier.uri>
<description.abstract>Small-scale clinical trials show that treatment of cystic fibrosis (CF) patients with ibuprofen, a nonsteroidal anti-inflammatory drug, improves the symptoms of CF and slows down the decline of lung function. Paradoxically, ibuprofen inhibits ligand-stimulated CF transmembrance conductance regulator (CFTR) activity. The aim of the present study was to investigate the effects of ibuprofen on CFTR function under different conditions. Patch-clamp recordings were performed in two lines of human airway epithelial cells: IB3-8-3-7 cells, which express wild-type CFTR; and IB3-1 cells, which express the variant CFTR with deletion of phenylalanine 580 (&#916;F580CFTR). Addition of ibuprofen to the extracellular solution caused a rapid inhibition of CFTR activity in IB3-8-3-7 cells in the presence of a high intracellular concentration of cAMP, whereas ibuprofen enhanced the CFTR conductance at low levels of cAMP. Introducing ibuprofen into the interior of cells occluded the enhancing effect of ibuprofen. Notably, the variant CFTR-mediated conductance was detected in IB3-1 cells treated with myoinositol and was enhanced by ibuprofen at endogenous levels of cAMP. In summary, nonsteroidal anti-inflammatory drugs increase the function of both wild-type cystic fibrosis transmembrane conductance regulator and the phenylalanine 580 deletion in cultured human airway epithelial cells at endogenous levels of cAMP. Copyright&#169;ERS Journals Ltd 2008.</description.abstract>
<language>eng</language>
<publisher>European Respiratory Society. The Journal&apos;s web site is located at http://erj.ersjournals.com</publisher>
<relation.ispartof>European Respiratory Journal</relation.ispartof>
<subject>Adenylate cyclase</subject>
<subject>Chloride channel</subject>
<subject>Forskolin</subject>
<subject>Lung epithelium</subject>
<subject>Perforated-patch recording</subject>
<subject.mesh>Anti-Inflammatory Agents, Non-Steroidal - pharmacology</subject.mesh>
<subject.mesh>Cystic Fibrosis - metabolism</subject.mesh>
<subject.mesh>Cystic Fibrosis Transmembrane Conductance Regulator - genetics - metabolism</subject.mesh>
<subject.mesh>Lung - drug effects - microbiology - pathology</subject.mesh>
<subject.mesh>Mutation</subject.mesh>
<title>Nonsteroidal anti-inflammatory drugs upregulate function of wild-type and mutant CFTR</title>
<type>Article</type>
<identifier.openurl>http://library.hku.hk:4550/resserv?sid=HKU:IR&amp;issn=0903-1936&amp;volume=32&amp;issue=2&amp;spage=334&amp;epage=343&amp;date=2008&amp;atitle=Nonsteroidal+anti-inflammatory+drugs+upregulate+function+of+wild-type+and+mutant+CFTR</identifier.openurl>
<description.nature>link_to_OA_fulltext</description.nature>
<identifier.doi>10.1183/09031936.00168007</identifier.doi>
<identifier.pmid>18385167</identifier.pmid>
<identifier.scopus>eid_2-s2.0-55149090254</identifier.scopus>
<relation.references>http://www.scopus.com/mlt/select.url?eid=2-s2.0-55149090254&amp;selection=ref&amp;src=s&amp;origin=recordpage</relation.references>
<identifier.volume>32</identifier.volume>
<identifier.issue>2</identifier.issue>
<identifier.spage>334</identifier.spage>
<identifier.epage>343</identifier.epage>
<identifier.isi>WOS:000258417000014</identifier.isi>
<publisher.place>Switzerland</publisher.place>
<bitstream.url>http://hub.hku.hk/bitstream/10722/143454/2/Content.txt</bitstream.url>
</item>
Author Affiliations
  1. University of Toronto Faculty of Medicine
  2. The University of Hong Kong
  3. University of Toronto
  4. Hospital for Sick Children University of Toronto
  5. Sunnybrook Health Sciences Centre