ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2009
Identification and functional characterization of the intermediate-conductance Ca(2+)-activated K(+) channel (IK-1) in biliary epithelium.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 34 citations in OpenAlex.
- Cholangiocyte biology in primary sclerosing cholangitis and other cholangiopathies: pathogenesis, clinical insights, and experimental tools.Physiological reviews · 2026Review
- Signaling through the interleukin-4 and interleukin-13 receptor complexes regulates cholangiocyte TMEM16A expression and biliary secretion.American journal of physiology. Gastrointestinal and liver physiology · 2020Article
- Pathobiology of biliary epithelia.Biochimica et biophysica acta. Molecular basis of disease · 2018Review
- Calcium Signaling in Liver Injury and Regeneration.Frontiers in medicine · 2018Review
- Apamin suppresses biliary fibrosis and activation of hepatic stellate cells.International journal of molecular medicine · 2017Article
- PKCα regulates TMEM16A-mediated Cl⁻ secretion in human biliary cells.American journal of physiology. Gastrointestinal and liver physiology · 2016Article
- Potassium channels in pancreatic duct epithelial cells: their role, function and pathophysiological relevance.Pflugers Archiv : European journal of physiology · 2015Review
- Mechanosensitive Cl- secretion in biliary epithelium mediated through TMEM16A.American journal of physiology. Gastrointestinal and liver physiology · 2013Article
- Physiology of cholangiocytes.Comprehensive Physiology · 2013Review
- Luminal cholinergic signalling in airway lining fluid: a novel mechanism for activating chloride secretion via Ca²⁺-dependent Cl⁻ and K⁺ channels.British journal of pharmacology · 2012Article
- K(Ca)2 channels: novel therapeutic targets for treating alcohol withdrawal and escalation of alcohol consumption.Alcohol (Fayetteville, N.Y.) · 2012Review
- Regulation of purinergic signaling in biliary epithelial cells by exocytosis of SLC17A9-dependent ATP-enriched vesicles.The Journal of biological chemistry · 2011Article
- Small conductance calcium-activated potassium type 2 channels regulate alcohol-associated plasticity of glutamatergic synapses.Biological psychiatry · 2011Article
- Identification and functional characterization of TMEM16A, a Ca2+-activated Cl- channel activated by extracellular nucleotides, in biliary epithelium.The Journal of biological chemistry · 2011Article
- Adenosine triphosphate release and purinergic (P2) receptor-mediated secretion in small and large mouse cholangiocytes.Hepatology (Baltimore, Md.) · 2010Article
- Endolymphatic sodium homeostasis by extramacular epithelium of the saccule.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
In the liver, adenosine triphosphate (ATP) is an extracellular signaling molecule that is released into bile and stimulates a biliary epithelial cell secretory response via engagement of apical P2 receptors. The molecular identities of the ion channels involved in ATP-mediated secretory responses have not been fully identified. Intermediate-conductance Ca(2+)-activated K(+) channels (IK) have been identified in biliary epithelium, but functional data are lacking. The aim of these studies therefore was to determine the location, function, and regulation of IK channels in biliary epithelial cells and to determine their potential contribution to ATP-stimulated secretion. Expression of IK-1 mRNA was found in both human Mz-Cha-1 biliary cells and polarized normal rat cholangiocyte (NRC) monolayers, and immunostaining revealed membrane localization with a predominant basolateral signal. In single Mz-Cha-1 cells, exposure to ATP activated K(+) currents, increasing current density from 1.6 +/- 0.1 to 7.6 +/- 0.8 pA/pF. Currents were dependent on intracellular Ca(2+) and sensitive to clotrimazole and TRAM-34 (specific IK channel inhibitors). Single-channel recording demonstrated that clotrimazole-sensitive K(+) currents had a unitary conductance of 46.2 +/- 1.5 pS, consistent with IK channels. In separate studies, 1-EBIO (an IK activator) stimulated K(+) currents in single cells that were inhibited by clotrimazole. In polarized NRC monolayers, ATP significantly increased transepithelial secretion which was inhibited by clotrimazole. Lastly, ATP-stimulated K(+) currents were inhibited by the P2Y receptor antagonist suramin and by the inositol 1,4,5-triphosphate (IP3) receptor inhibitor 2-APB. Together these studies demonstrate that IK channels are present in biliary epithelial cells and contribute to ATP-stimulated secretion through a P2Y-IP3 receptor pathway.
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