ArticleRespiratory research2006
Activation of chloride transport in CF airway epithelial cell lines and primary CF nasal epithelial cells by S-nitrosoglutathione.
Article in Respiratory research, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 36 citations in OpenAlex.
- S-nitrosothiols signaling in cystic fibrosis airways.Journal of biosciences · 2021Review
- Article
- Augmentation of CFTR maturation by S-nitrosoglutathione reductase.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Correction of defective CFTR/ENaC function and tightness of cystic fibrosis airway epithelium by amniotic mesenchymal stromal (stem) cells.Journal of cellular and molecular medicine · 2014Article
- S-Nitrosothiols increases cystic fibrosis transmembrane regulator expression and maturation in the cell surface.Biochemical and biophysical research communications · 2014Article
- Involvement of the cystic fibrosis transmembrane conductance regulator in the acidosis-induced efflux of ATP from rat skeletal muscle.The Journal of physiology · 2010Article
- Metabolomic profiling reveals biochemical pathways and biomarkers associated with pathogenesis in cystic fibrosis cells.The Journal of biological chemistry · 2010Article
- Hsp 70/Hsp 90 organizing protein as a nitrosylation target in cystic fibrosis therapy.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Protein processing and inflammatory signaling in Cystic Fibrosis: challenges and therapeutic strategies.Current molecular medicine · 2010Review
- Morphological and functional heterogeneity of the mouse intrahepatic biliary epithelium.Laboratory investigation; a journal of technical methods and pathology · 2009Article
- Glutathione dysregulation and the etiology and progression of human diseases.Biological chemistry · 2009Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundIt has been suggested that low microM concentrations of S-nitrosoglutathione (GSNO), an endogenous bronchodilator, may promote maturation of the defective cystic fibrosis (CF) transmembrane conductance regulator (CFTR). Because nitric oxide (NO) and GSNO levels appear to be low in the CF airway, there is an interest in the possibility that GSNO replacement could be of therapeutic benefit in CF.
methodsThe effect of GSNO on chloride (Cl-) transport was investigated in primary nasal epithelial cells obtained from CF patients homozygous for the delF508 mutation, as well as in two CF cell lines (CFBE and CFSME), using both a fluorescent Cl- indicator and X-ray microanalysis. Maturation of delF508 CFTR was determined by immunoblotting.
resultsTreatment with 60 microM GSNO for 4 hours increased cAMP-induced chloride efflux in nasal epithelial cells from 18 out of 21 CF patients, but did not significantly affect Cl- efflux in cells from healthy controls. This Cl- efflux was confirmed by measurements with a fluorescent Cl- indicator in the CFBE and CFSME cell lines. The effect of GSNO on Cl- efflux in CFBE cells could be inhibited both by a specific thiazolidinone CFTR inhibitor (CFTRinh-172) and by 4,4'-diisothiocyanatodihydrostilbene-2,2'-disulfonic acid (H2DIDS). X-ray microanalysis showed that, following 4 hours incubation with 60 microM GSNO, cAMP agonists caused a decrease in the cellular Cl- concentration in CFBE cells, corresponding to Cl- efflux. GSNO exposure resulted in an increase in the protein expression and maturation, as shown by immunoblot analysis. GSNO did not increase the cytosolic Ca2+ concentration in cultured airway epithelial cells.
conclusionPrevious studies have suggested that treatment with GSNO promotes maturation of delF508-CFTR, consistent with our results in this study. Here we show that GSNO increases chloride efflux, both in the two CF cell lines and in primary nasal epithelial cells from delF508-CF patients. This effect is at least in part mediated by CFTR. GSNO may be a candidate for pharmacological treatment of the defective chloride transport in CF epithelial cells.
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