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Article: Nonsteroidal anti-inflammatory drugs upregulate function of wild-type and mutant CFTR

TitleNonsteroidal anti-inflammatory drugs upregulate function of wild-type and mutant CFTR
Authors
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
Citation
European Respiratory Journal, 2008, v. 32 n. 2, p. 334-343 How to Cite?
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 (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.
Persistent Identifierhttp://hdl.handle.net/10722/143454
ISSN
2013 Impact Factor: 7.125
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLi, Jen_HK
dc.contributor.authorXiang, YYen_HK
dc.contributor.authorYe, Len_HK
dc.contributor.authorTsui, LCen_HK
dc.contributor.authorMacDonald, JFen_HK
dc.contributor.authorHu, Jen_HK
dc.contributor.authorLu, WYen_HK
dc.date.accessioned2011-11-25T08:30:12Z-
dc.date.available2011-11-25T08:30:12Z-
dc.date.issued2008en_HK
dc.identifier.citationEuropean Respiratory Journal, 2008, v. 32 n. 2, p. 334-343en_HK
dc.identifier.issn0903-1936en_HK
dc.identifier.urihttp://hdl.handle.net/10722/143454-
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.en_HK
dc.languageeng-
dc.publisherEuropean Respiratory Society. The Journal's web site is located at http://erj.ersjournals.comen_HK
dc.relation.ispartofEuropean Respiratory Journalen_HK
dc.subjectAdenylate cyclaseen_HK
dc.subjectChloride channelen_HK
dc.subjectForskolinen_HK
dc.subjectLung epitheliumen_HK
dc.subjectPerforated-patch recordingen_HK
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.titleNonsteroidal anti-inflammatory drugs upregulate function of wild-type and mutant CFTRen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0903-1936&volume=32&issue=2&spage=334&epage=343&date=2008&atitle=Nonsteroidal+anti-inflammatory+drugs+upregulate+function+of+wild-type+and+mutant+CFTR-
dc.identifier.emailTsui, LC: tsuilc@hkucc.hku.hken_HK
dc.identifier.authorityTsui, LC=rp00058en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1183/09031936.00168007en_HK
dc.identifier.pmid18385167-
dc.identifier.scopuseid_2-s2.0-55149090254en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-55149090254&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume32en_HK
dc.identifier.issue2en_HK
dc.identifier.spage334en_HK
dc.identifier.epage343en_HK
dc.identifier.isiWOS:000258417000014-
dc.publisher.placeSwitzerlanden_HK
dc.identifier.scopusauthoridLi, J=8956464300en_HK
dc.identifier.scopusauthoridXiang, YY=25646942700en_HK
dc.identifier.scopusauthoridYe, L=35504324300en_HK
dc.identifier.scopusauthoridTsui, LC=7102754167en_HK
dc.identifier.scopusauthoridMacDonald, JF=7401438826en_HK
dc.identifier.scopusauthoridHu, J=7406420553en_HK
dc.identifier.scopusauthoridLu, WY=25646631100en_HK

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