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- Publisher Website: 10.1183/09031936.00168007
- Scopus: eid_2-s2.0-55149090254
- PMID: 18385167
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Article: Nonsteroidal anti-inflammatory drugs upregulate function of wild-type and mutant CFTR
Title | Nonsteroidal anti-inflammatory drugs upregulate function of wild-type and mutant CFTR |
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Authors | |
Keywords | Adenylate cyclase Chloride channel Forskolin Lung epithelium Perforated-patch recording |
Issue Date | 2008 |
Publisher | European 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 Identifier | http://hdl.handle.net/10722/143454 |
ISSN | 2023 Impact Factor: 16.6 2023 SCImago Journal Rankings: 3.810 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Li, J | en_HK |
dc.contributor.author | Xiang, YY | en_HK |
dc.contributor.author | Ye, L | en_HK |
dc.contributor.author | Tsui, LC | en_HK |
dc.contributor.author | MacDonald, JF | en_HK |
dc.contributor.author | Hu, J | en_HK |
dc.contributor.author | Lu, WY | en_HK |
dc.date.accessioned | 2011-11-25T08:30:12Z | - |
dc.date.available | 2011-11-25T08:30:12Z | - |
dc.date.issued | 2008 | en_HK |
dc.identifier.citation | European Respiratory Journal, 2008, v. 32 n. 2, p. 334-343 | en_HK |
dc.identifier.issn | 0903-1936 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/143454 | - |
dc.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 (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.language | eng | - |
dc.publisher | European Respiratory Society. The Journal's web site is located at http://erj.ersjournals.com | en_HK |
dc.relation.ispartof | European Respiratory Journal | en_HK |
dc.subject | Adenylate cyclase | en_HK |
dc.subject | Chloride channel | en_HK |
dc.subject | Forskolin | en_HK |
dc.subject | Lung epithelium | en_HK |
dc.subject | Perforated-patch recording | en_HK |
dc.subject.mesh | Anti-Inflammatory Agents, Non-Steroidal - pharmacology | - |
dc.subject.mesh | Cystic Fibrosis - metabolism | - |
dc.subject.mesh | Cystic Fibrosis Transmembrane Conductance Regulator - genetics - metabolism | - |
dc.subject.mesh | Lung - drug effects - microbiology - pathology | - |
dc.subject.mesh | Mutation | - |
dc.title | Nonsteroidal anti-inflammatory drugs upregulate function of wild-type and mutant CFTR | en_HK |
dc.type | Article | en_HK |
dc.identifier.openurl | http://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.email | Tsui, LC: tsuilc@hkucc.hku.hk | en_HK |
dc.identifier.authority | Tsui, LC=rp00058 | en_HK |
dc.description.nature | link_to_OA_fulltext | - |
dc.identifier.doi | 10.1183/09031936.00168007 | en_HK |
dc.identifier.pmid | 18385167 | - |
dc.identifier.scopus | eid_2-s2.0-55149090254 | en_HK |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-55149090254&selection=ref&src=s&origin=recordpage | en_HK |
dc.identifier.volume | 32 | en_HK |
dc.identifier.issue | 2 | en_HK |
dc.identifier.spage | 334 | en_HK |
dc.identifier.epage | 343 | en_HK |
dc.identifier.isi | WOS:000258417000014 | - |
dc.publisher.place | Switzerland | en_HK |
dc.identifier.scopusauthorid | Li, J=8956464300 | en_HK |
dc.identifier.scopusauthorid | Xiang, YY=25646942700 | en_HK |
dc.identifier.scopusauthorid | Ye, L=35504324300 | en_HK |
dc.identifier.scopusauthorid | Tsui, LC=7102754167 | en_HK |
dc.identifier.scopusauthorid | MacDonald, JF=7401438826 | en_HK |
dc.identifier.scopusauthorid | Hu, J=7406420553 | en_HK |
dc.identifier.scopusauthorid | Lu, WY=25646631100 | en_HK |
dc.identifier.issnl | 0903-1936 | - |