ArticleRespiratory research2008
Abnormal spatial diffusion of Ca2+ in F508del-CFTR airway epithelial cells.
Article in Respiratory research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 37 citations in OpenAlex.
- A Laminar Microfluidic Platform for Probing the Effects of Spatially Heterogeneous Drug Distributions.Micromachines · 2026Article
- Beyond the mutations: spatiotemporal regulation of CFTR by cAMP and calcium signaling in epithelial physiology and cystic fibrosis.Cellular & molecular biology letters · 2025Review
- Recovery of ΔF508-CFTR Function by Citrate.Nutrients · 2022Article
- Impaired regulation of PMCA activity by defective CFTR expression promotes epithelial cell damage in alcoholic pancreatitis and hepatitis.Cellular and molecular life sciences : CMLS · 2022Article
- Integrative chemogenomic analysis identifies small molecules that partially rescue ΔF508-CFTR for cystic fibrosis.CPT: pharmacometrics & systems pharmacology · 2021Article
- Update on Calcium Signaling in Cystic Fibrosis Lung Disease.Frontiers in pharmacology · 2021Review
- The Role of Specialized Pro-Resolving Mediators in Cystic Fibrosis Airways Disease.Frontiers in pharmacology · 2020Review
- Inhibition of calpain 1 restores plasma membrane stability to pharmacologically rescued Phe508del-CFTR variant.The Journal of biological chemistry · 2019Article
- Cystic Fibrosis of the Pancreas: The Role of CFTR Channel in the Regulation of Intracellular CaFrontiers in physiology · 2018Review
- Function and regulation of TRPM7, as well as intracellular magnesium content, are altered in cells expressing ΔF508-CFTR and G551D-CFTR.Cellular and molecular life sciences : CMLS · 2016Article
- Dysregulated Chemokine Signaling in Cystic Fibrosis Lung Disease: A Potential Therapeutic Target.Current drug targets · 2016Review
- The impact of Cystic Fibrosis Transmembrane Regulator Disruption on cardiac function and stress response.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2016Article
- Cystic fibrosis bronchial epithelial cells are lipointoxicated by membrane palmitate accumulation.PloS one · 2014Article
- Calpain inhibition promotes the rescue of F(508)del-CFTR in PBMC from cystic fibrosis patients.PloS one · 2013Article
- Insulin production and resistance in cystic fibrosis: effect of age, disease activity, and genotype.Journal of endocrinological investigation · 2012Article
- Article
- Ouabain Mimics Low Temperature Rescue of F508del-CFTR in Cystic Fibrosis Epithelial Cells.Frontiers in pharmacology · 2012Article
- Enhanced Ca2+ entry due to Orai1 plasma membrane insertion increases IL-8 secretion by cystic fibrosis airways.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2011Article
- Calcium-modulated chloride pathways contribute to chloride flux in murine cystic fibrosis-affected macrophages.Pediatric research · 2011Article
- CFTR and Ca Signaling in Cystic Fibrosis.Frontiers in pharmacology · 2011Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIn airway epithelial cells, calcium mobilization can be elicited by selective autocrine and/or paracrine activation of apical or basolateral membrane heterotrimeric G protein-coupled receptors linked to phospholipase C (PLC) stimulation, which generates inositol 1,4,5-trisphosphate (IP3) and 1,2-diacylglycerol (DAG) and induces Ca2+ release from endoplasmic reticulum (ER) stores.
methodsIn the present study, we monitored the cytosolic Ca2+ transients using the UV light photolysis technique to uncage caged Ca2+ or caged IP3 into the cytosol of loaded airway epithelial cells of cystic fibrosis (CF) and non-CF origin. We compared in these cells the types of Ca2+ receptors present in the ER, and measured their Ca2+ dependent activity before and after correction of F508del-CFTR abnormal trafficking either by low temperature or by the pharmacological corrector miglustat (N-butyldeoxynojirimycin).
resultsWe showed reduction of the inositol 1,4,5-trisphosphate receptors (IP3R) dependent-Ca2+ response following both correcting treatments compared to uncorrected cells in such a way that Ca2+ responses (CF+treatment vs wild-type cells) were normalized. This normalization of the Ca2+ rate does not affect the activity of Ca2+-dependent chloride channel in miglustat-treated CF cells. Using two inhibitors of IP3R1, we observed a decrease of the implication of IP3R1 in the Ca2+ response in CF corrected cells. We observed a similar Ca2+ mobilization between CF-KM4 cells and CFTR-cDNA transfected CF cells (CF-KM4-reverted). When we restored the F508del-CFTR trafficking in CFTR-reverted cells, the specific IP3R activity was also reduced to a similar level as in non CF cells. At the structural level, the ER morphology of CF cells was highly condensed around the nucleus while in non CF cells or corrected CF cells the ER was extended at the totality of cell.
conclusionThese results suggest reversal of the IP3R dysfunction in F508del-CFTR epithelial cells by correction of the abnormal trafficking of F508del-CFTR in cystic fibrosis cells. Moreover, using CFTR cDNA-transfected CF cells, we demonstrated that abnormal increase of IP3R Ca2+ release in CF human epithelial cells could be the consequence of F508del-CFTR retention in ER compartment.
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