ArticleBiochemical and biophysical research communications2012
Lubiprostone activates CFTR, but not ClC-2, via the prostaglandin receptor (EP(4)).
Article in Biochemical and biophysical research communications, 2012. 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, 40 citations in OpenAlex.
- Chloride channels and mast cell function: pioneering new frontiers in IBD therapy.Molecular and cellular biochemistry · 2025Review
- Lubiprostone Improves Distal Segment-Specific Colonic Contractions through TRPC4 Activation Stimulated by EP3 Prostanoid Receptor.Pharmaceuticals (Basel, Switzerland) · 2024Article
- The ClC-2 Chloride Channel Activator, Lubiprostone, Improves Intestinal Barrier Function in Biopsies from Crohn's Disease but Not Ulcerative Colitis Patients.Pharmaceutics · 2023Article
- Lubiprostone is non-selective activator of cAMP-gated ion channels and Clc-2 has a minor role in its prosecretory effect in intestinal epithelial cells.Molecular pharmacology · 2022Article
- Intestinal secretory mechanisms and diarrhea.American journal of physiology. Gastrointestinal and liver physiology · 2022Review
- Receptor-mediated activation of CFTR via prostaglandin signaling pathways in the airway.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- Development and validation of a potent and specific inhibitor for the CLC-2 chloride channel.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Article
- Lubiprostone protects esophageal mucosa from acid injury in porcine esophagus.American journal of physiology. Gastrointestinal and liver physiology · 2020Article
- Herbal components of Japanese Kampo medicines exert laxative actions in colonic epithelium cells via activation of BK and CFTR channels.Scientific reports · 2019Article
- Cellular mechanism for herbal medicine Junchoto to facilitate intestinal ClJournal of natural medicines · 2018Article
- Recent advances in understanding and managing chronic constipation.F1000Research · 2018Review
- Research and progress on ClC‑2 (Review).Molecular medicine reports · 2017Review
- Luminally Acting Agents for Constipation Treatment: A Review Based on Literatures and Patents.Frontiers in pharmacology · 2017Review
- Current developments in pharmacological therapeutics for chronic constipation.Acta pharmaceutica Sinica. B · 2015Review
- Treatment of Chronic Constipation: Prescription Medications and Surgical Therapies.Gastroenterology & hepatology · 2015Article
- Effects of lubiprostone on pacemaker activity of interstitial cells of cajal from the mouse colon.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2014Article
- The use of non-narcotic pain medication in pediatric gastroenterology.Paediatric drugs · 2014Review
- Aqueous cigarette smoke extract induces a voltage-dependent inhibition of CFTR expressed in Xenopus oocytes.American journal of physiology. Lung cellular and molecular physiology · 2014Article
- Physiology, signaling, and pharmacology of opioid receptors and their ligands in the gastrointestinal tract: current concepts and future perspectives.Journal of gastroenterology · 2014Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The goal of this study was to determine the mechanism of lubiprostone activation of epithelial chloride transport. Lubiprostone is a bicyclic fatty acid approved for the treatment of constipation [1]. There is uncertainty, however, as to how lubiprostone increases epithelial chloride transport. Direct stimulation of ClC-2 and CFTR chloride channels as well as stimulation of these channels via the EP(4) receptor has been described [2-5]. To better define this mechanism, two-electrode voltage clamp was used to assay Xenopus oocytes expressing ClC-2, with or without co-expression of the EP(4) receptor or β adrenergic receptor (βAR), for changes in conductance elicited by lubiprostone. Oocytes co-expressing CFTR and either βAR or the EP(4) receptor were also studied. In oocytes co-expressing ClC-2 and βAR conductance was stimulated by hyperpolarization and acidic pH (pH = 6), but there was no response to the β adrenergic agonist, isoproterenol. Oocytes expressing ClC-2 only or co-expressing ClC-2 and EP(4) did not respond to the presence of 0.1, 1, or 10 μM lubiprostone in the superperfusate. Oocytes co-expressing CFTR and βAR did not respond to hyperpolarization, acidic pH, or 1 μM lubiprostone. However, conductance was elevated by isoproterenol and inhibited by CFTR(inh)172. Co-expression of CFTR and EP(4) resulted in lubiprostone-stimulated conductance, which was also sensitive to CFTR(inh)172. The EC(50) for lubiprostone mediated CFTR activation was ~10 nM. These results demonstrate no direct action of lubiprostone on either ClC-2 or CFTR channels expressed in oocytes. However, the results confirm that CFTR can be activated by lubiprostone via the EP(4) receptor in oocytes.
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Registered trials
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