ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2008
Extracellular nucleotides stimulate Cl- currents in biliary epithelia through receptor-mediated IP3 and Ca2+ release.
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 22 papers.
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Who cites it
22 citing papers in PubMed, 41 citations in OpenAlex.
- P2Y2 purinergic receptor gene deletion protects mice from bacterial endotoxin and sepsis-associated liver injury and mortality.American journal of physiology. Gastrointestinal and liver physiology · 2023Article
- Active enterohepatic cycling is not required for the choleretic actions of 24-norUrsodeoxycholic acid in mice.JCI insight · 2023Article
- Conjunctival Fluid Secretion Impairment via CaCC-CFTR Dysfunction Is the Key Mechanism in Environmental Dry Eye.International journal of molecular sciences · 2022Article
- Identification of the chloride channel, leucine-rich repeat-containing protein 8, subfamily a (LRRC8A), in mouse cholangiocytes.Hepatology (Baltimore, Md.) · 2022Article
- Piezo1-Pannexin1 complex couples force detection to ATP secretion in cholangiocytes.The Journal of general physiology · 2021Article
- 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
- Mechanosensor transient receptor potential vanilloid member 4 (TRPV4) regulates mouse cholangiocyte secretion and bile formation.American journal of physiology. Gastrointestinal and liver physiology · 2020Article
- Pathophysiology of Cystic Fibrosis Liver Disease: A Channelopathy Leading to Alterations in Innate Immunity and in Microbiota.Cellular and molecular gastroenterology and hepatology · 2019Review
- Bile acids stimulate cholangiocyte fluid secretion by activation of transmembrane member 16A ClHepatology (Baltimore, Md.) · 2018Article
- Pathobiology of biliary epithelia.Biochimica et biophysica acta. Molecular basis of disease · 2018Review
- Regulation of mechanosensitive biliary epithelial transport by the epithelial Na(+) channel.Hepatology (Baltimore, Md.) · 2016Article
- PKCα regulates TMEM16A-mediated Cl⁻ secretion in human biliary cells.American journal of physiology. Gastrointestinal and liver physiology · 2016Article
- Calcium signaling and the secretory activity of bile duct epithelia.Cell calcium · 2014Review
- Purinergic signalling in the gastrointestinal tract and related organs in health and disease.Purinergic signalling · 2014Review
- Apical localization of inositol 1,4,5-trisphosphate receptors is independent of extended synaptotagmins in hepatocytes.PloS one · 2014Article
- Physiology of cholangiocytes.Comprehensive Physiology · 2013Review
- Mechanosensitive Cl- secretion in biliary epithelium mediated through TMEM16A.American journal of physiology. Gastrointestinal and liver physiology · 2013Article
- Differential effects of extracellular ATP on chloride transport in cortical collecting duct cells.American journal of physiology. Renal physiology · 2012Article
- Regulation of purinergic signaling in biliary epithelial cells by exocytosis of SLC17A9-dependent ATP-enriched vesicles.The Journal of biological chemistry · 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
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Extracellular ATP regulates bile formation by binding to P2 receptors on cholangiocytes and stimulating transepithelial Cl(-) secretion. However, the specific signaling pathways linking receptor binding to Cl(-) channel activation are not known. Consequently, the aim of these studies in human Mz-Cha-1 biliary cells and normal rat cholangiocyte monolayers was to assess the intracellular pathways responsible for ATP-stimulated increases in intracellular Ca(2+) concentration ([Ca(2+)](i)) and membrane Cl(-) permeability. Exposure of cells to ATP resulted in a rapid increase in [Ca(2+)](i) and activation of membrane Cl(-) currents; both responses were abolished by prior depletion of intracellular Ca(2+). ATP-stimulated Cl(-) currents demonstrated mild outward rectification, reversal at E(Cl(-)), and a single-channel conductance of approximately 17 pS, where E is the equilibrium potential. The conductance response to ATP was inhibited by the Cl(-) channel inhibitors NPPB and DIDS but not the CFTR inhibitor CFTR(inh)-172. Both ATP-stimulated increases in [Ca(2+)](i) and Cl(-) channel activity were inhibited by the P2Y receptor antagonist suramin. The PLC inhibitor U73122 and the inositol 1,4,5-triphosphate (IP3) receptor inhibitor 2-APB both blocked the ATP-stimulated increase in [Ca(2+)](i) and membrane Cl(-) currents. Intracellular dialysis with purified IP3 activated Cl(-) currents with identical properties to those activated by ATP. Exposure of normal rat cholangiocyte monolayers to ATP increased short-circuit currents (I(sc)), reflecting transepithelial secretion. The I(sc) was unaffected by CFTR(inh)-172 but was significantly inhibited by U73122 or 2-APB. In summary, these findings indicate that the apical P2Y-IP3 receptor signaling complex is a dominant pathway mediating biliary epithelial Cl(-) transport and, therefore, may represent a potential target for increasing secretion in the treatment of cholestatic liver disease.
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