ArticleAmerican journal of physiology. Lung cellular and molecular physiology2008
Lubiprostone activates non-CFTR-dependent respiratory epithelial chloride secretion in cystic fibrosis mice.
Article in American journal of physiology. Lung cellular and molecular physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 45 citations in OpenAlex.
- Synthesis of ionizable lipopolymers using split-Ugi reaction for pulmonary delivery of various size RNAs and gene editing.Nature communications · 2025Article
- Receptor-mediated activation of CFTR via prostaglandin signaling pathways in the airway.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- Prognosis-Based Early Intervention Strategies to Resolve Exacerbation and Progressive Lung Function Decline in Cystic Fibrosis.Journal of personalized medicine · 2021Article
- Assessment of Lentiviral Vector Mediated CFTR Correction in Mice Using an Improved RapidFrontiers in pharmacology · 2021Article
- Negative chronotropic and inotropic effects of lubiprostone on iPS cell-derived cardiomyocytes via activation of CFTR.BMC complementary medicine and therapies · 2020Article
- Lipid Nanoparticle-Delivered Chemically Modified mRNA Restores Chloride Secretion in Cystic Fibrosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2018Article
- Direct interactions between ENaC gamma subunit and ClCN2 in cystic fibrosis epithelial cells.Physiological reports · 2015Article
- Role of lubiprostone on gastrointestinal motility.Journal of neurogastroenterology and motility · 2013Article
- Lubiprostone decreases mouse colonic inner mucus layer thickness and alters intestinal microbiota.Digestive diseases and sciences · 2013Article
- Dual activation of CFTR and CLCN2 by lubiprostone in murine nasal epithelia.American journal of physiology. Lung cellular and molecular physiology · 2013Article
- Lubiprostone activates CFTR, but not ClC-2, via the prostaglandin receptor (EP(4)).Biochemical and biophysical research communications · 2012Article
- Cystic fibrosis growth retardation is not correlated with loss of Cftr in the intestinal epithelium.American journal of physiology. Gastrointestinal and liver physiology · 2011Article
- Lubiprostone targets prostanoid EP₄ receptors in ovine airways.British journal of pharmacology · 2011Article
- Lubiprostone: evaluation of the newest medication for the treatment of adult women with constipation-predominant irritable bowel syndrome.International journal of women's health · 2010Article
- 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
- Lubiprostone: clinical applications beyond constipation.World journal of gastroenterology · 2009Article
- Cystic fibrosis and estrogens: a perfect storm.The Journal of clinical investigation · 2008Article
- ClC-2 regulation of intestinal barrier function: Translation of basic science to therapeutic target.Tissue barriersReview
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Periciliary fluid balance is maintained by the coordination of sodium and chloride channels in the apical membranes of the airways. In the absence of the cystic fibrosis transmembrane regulator (CFTR), chloride secretion is diminished and sodium reabsorption exaggerated. ClC-2, a pH- and voltage-dependent chloride channel, is present on the apical membranes of airway epithelial cells. We hypothesized that ClC-2 agonists would provide a parallel pathway for chloride secretion. Using nasal potential difference (NPD) measurements, we quantified lubiprostone-mediated Cl(-) transport in sedated cystic fibrosis null (gut-corrected), C57Bl/6, and A/J mice during nasal perfusion of lubiprostone (a putative ClC-2 agonist). Baseline, amiloride-inhibited, chloride-free gluconate-substituted Ringer with amiloride and low-chloride Ringer plus lubiprostone (at increasing concentrations of lubiprostone) were perfused, and the NPD was continuously recorded. A clear dose-response relationship was detected in all murine strains. The magnitude of the NPD response to 20 muM lubiprostone was -5.8 +/- 2.1 mV (CF, n = 12), -8.1 +/- 2.6 mV (C57Bl/6 wild-type, n = 12), and -5.3 +/- 1.2 mV (AJ wild-type, n = 8). A cohort of ClC-2 knockout mice did not respond to 20 muM lubiprostone (n = 6, P = 0.27). In C57Bl/6 mice, inhibition of CFTR with topical application of CFTR inhibitor-172 did not abolish the lubiprostone response, thus confirming the response seen is independent of CFTR regulation. RT-PCR confirmed expression of ClC-2 mRNA in murine lung homogenate. The direct application of lubiprostone in the CF murine nasal airway restores nearly normal levels of chloride secretion in nasal epithelia.
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