ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2008
A synthetic prostone activates apical chloride channels in A6 epithelial cells.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
42 citing papers in PubMed, 69 citations in OpenAlex.
- Effect of a chloride channel activator, lubiprostone, on colonic sensory and motor functions in healthy subjects.American journal of physiology. Gastrointestinal and liver physiology · 2009Trial
- Chloride channels and mast cell function: pioneering new frontiers in IBD therapy.Molecular and cellular biochemistry · 2025Review
- 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
- Receptor-mediated activation of CFTR via prostaglandin signaling pathways in the airway.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- Functional Role of Basolateral ClC-2 Channels in the Regulation of Duodenal Anion Secretion in Mice.Digestive diseases and sciences · 2019Article
- Chronic stress and intestinal permeability: Lubiprostone regulates glucocorticoid receptor-mediated changes in colon epithelial tight junction proteins, barrier function, and visceral pain in the rodent and human.Neurogastroenterology and motility · 2019Article
- Article
- Research and progress on ClC‑2 (Review).Molecular medicine reports · 2017Review
- Alveolar nonselective channels are ASIC1a/α-ENaC channels and contribute to AFC.American journal of physiology. Lung cellular and molecular physiology · 2017Article
- Opioids and GI Motility-Friend or Foe?Current treatment options in gastroenterology · 2016Review
- The sodium chloride cotransporter (NCC) and epithelial sodium channel (ENaC) associate.The Biochemical journal · 2016Article
- Prolactin stimulates sodium and chloride ion channels in A6 renal epithelial cells.American journal of physiology. Renal physiology · 2015Article
- A comparison of linaclotide and lubiprostone dosing regimens on ion transport responses in human colonic mucosa.Pharmacology research & perspectives · 2015Article
- Lubiprostone in constipation: clinical evidence and place in therapy.Therapeutic advances in chronic disease · 2015Review
- Treatment of Chronic Constipation: Prescription Medications and Surgical Therapies.Gastroenterology & hepatology · 2015Article
- Distinct action of flavonoids, myricetin and quercetin, on epithelial Cl⁻ secretion: useful tools as regulators of Cl⁻ secretion.BioMed research international · 2014Article
- Methadone but not morphine inhibits lubiprostone-stimulated Cl- currents in T84 intestinal cells and recombinant human ClC-2, but not CFTR Cl- currents.Cell biochemistry and biophysics · 2013Article
- Dual activation of CFTR and CLCN2 by lubiprostone in murine nasal epithelia.American journal of physiology. Lung cellular and molecular physiology · 2013Article
- Lubiprostone decreases mouse colonic inner mucus layer thickness and alters intestinal microbiota.Digestive diseases and sciences · 2013Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The bicyclic fatty acid lubiprostone (formerly known as SPI-0211) activates two types of anion channels in A6 cells. Both channel types are rarely, if ever, observed in untreated cells. The first channel type was activated at low concentrations of lubiprostone (<100 nM) in >80% of cell-attached patches and had a unit conductance of approximately 3-4 pS. The second channel type required higher concentrations (>100 nM) of lubiprostone to activate, was observed in approximately 30% of patches, and had a unit conductance of 8-9 pS. The properties of the first type of channel were consistent with ClC-2 and the second with CFTR. ClC-2's unit current strongly inwardly rectified that could be best fit by models of the channel with multiple energy barrier and multiple anion binding sites in the conductance pore. The open probability and mean open time of ClC-2 was voltage dependent, decreasing dramatically as the patches were depolarized. The order of anion selectivity for ClC-2 was Cl > Br > NO(3) > I > SCN, where SCN is thiocyanate. ClC-2 was a "double-barreled" channel favoring even numbers of levels over odd numbers as if the channel protein had two conductance pathways that opened independently of one another. The channel could be, at least, partially blocked by glibenclamide. The properties of the channel in A6 cells were indistinguishable from ClC-2 channels stably transfected in HEK293 cells. CFTR in the patches had a selectivity of Cl > Br >> NO(3) congruent with SCN congruent with I. It outwardly rectified as expected for a single-site anion channel. Because of its properties, ClC-2 is uniquely suitable to promote anion secretion with little anion reabsorption. CFTR, on the other hand, could promote either reabsorption or secretion depending on the anion driving forces.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.