ArticleBritish journal of pharmacology2007
Chloride transporting capability of Calu-3 epithelia following persistent knockdown of the cystic fibrosis transmembrane conductance regulator, CFTR.
Article in British journal of pharmacology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
21 citing papers in PubMed.
- A Peptide Nucleic Acid (PNA) Masking the miR-145-5p Binding Site of the 3'UTR of the Cystic Fibrosis Transmembrane Conductance Regulator (Molecules (Basel, Switzerland) · 2020Article
- Most bicarbonate secretion by Calu-3 cells is mediated by CFTR and independent of pendrin.Physiological reports · 2018Article
- Mechanosensitivity of wild-type and G551D cystic fibrosis transmembrane conductance regulator (CFTR) controls regulatory volume decrease in simple epithelia.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
- Pulmonary epithelial barrier function: some new players and mechanisms.American journal of physiology. Lung cellular and molecular physiology · 2015Review
- A comparison of linaclotide and lubiprostone dosing regimens on ion transport responses in human colonic mucosa.Pharmacology research & perspectives · 2015Article
- Protein phosphatase 1 coordinates CFTR-dependent airway epithelial HCO3- secretion by reciprocal regulation of apical and basolateral membrane Cl(-)-HCO3- exchangers.British journal of pharmacology · 2013Article
- Lubiprostone decreases mouse colonic inner mucus layer thickness and alters intestinal microbiota.Digestive diseases and sciences · 2013Article
- Bicarbonate-dependent chloride transport drives fluid secretion by the human airway epithelial cell line Calu-3.The Journal of physiology · 2012Article
- Lubiprostone activates CFTR, but not ClC-2, via the prostaglandin receptor (EP(4)).Biochemical and biophysical research communications · 2012Article
- Mutation conferring apical-targeting motif on AE1 exchanger causes autosomal dominant distal RTA.Journal of the American Society of Nephrology : JASN · 2012Article
- Article
- Novel role for pendrin in orchestrating bicarbonate secretion in cystic fibrosis transmembrane conductance regulator (CFTR)-expressing airway serous cells.The Journal of biological chemistry · 2011Article
- Lubiprostone activates Cl- secretion via cAMP signaling and increases membrane CFTR in the human colon carcinoma cell line, T84.Digestive diseases and sciences · 2011Article
- Lubiprostone targets prostanoid EP₄ receptors in ovine airways.British journal of pharmacology · 2011Article
- Lubiprostone ameliorates the cystic fibrosis mouse intestinal phenotype.BMC gastroenterology · 2010Article
- Lubiprostone stimulates secretion from tracheal submucosal glands of sheep, pigs, and humans.American journal of physiology. Lung cellular and molecular physiology · 2009Article
- Salmeterol restores secretory functions in cystic fibrosis airway submucosal gland serous cells.American journal of respiratory cell and molecular biology · 2009Article
- Hypoxia inducible factor-1 (HIF-1)-mediated repression of cystic fibrosis transmembrane conductance regulator (CFTR) in the intestinal epithelium.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2009Article
- Lubiprostone activates non-CFTR-dependent respiratory epithelial chloride secretion in cystic fibrosis mice.American journal of physiology. Lung cellular and molecular physiology · 2008Article
- Cystic Fibrosis: The Mechanisms of Pathogenesis of an Inherited Lung Disorder.Drug discovery today. Disease mechanisms · 2007Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeCalu-3 cells are derived from serous cells of human lung submucosal glands, a prime target for therapy in cystic fibrosis (CF). Calu-3 cells can be cultured to form epithelia capable of transepithelial transport of chloride. A CF Calu-3 cell is not available. EXPERIMENTAL APPROACH: A retroviral vector was used to cause persistent down regulation of CFTR using siRNA methodology, in Calu-3 cells. A Calu-3 cell line with CFTR content less than 5% of the original line has been established. Epithelia grown using the modified cells have been used in comparative studies of transporting capability. KEY
resultsAll aspects of cAMP activated chloride secretion were attenuated in the epithelia with reduced CFTR content. However transporting capability was reduced less than the CFTR content. From studies with the CFTR channel inhibitor, GlyH-101, it was concluded that wild type Calu-3 cells have a reserve of CFTR channels not located in the membrane, but available for replacement, while in the modified Calu-3 cell line there was little or no reserve. Lubiprostone, a putative ClC-2 activator, increased transepithelial chloride secretion in both modified and wild type Calu-3 epithelia. Modified Calu-3 epithelia with the residual CFTR currents blocked with GlyH-101 responded equally well to lubiprostone as those without the blocking agent. CONCLUSIONS AND IMPLICATIONS: It appears that lubiprostone is capable of stimulating a non-CFTR dependent transepithelial chloride secretion in Calu-3 monolayers, with obvious implications for CF therapy. Cell lines, however, do not always reflect the behaviour of the native tissue with integrity.
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