| Damage to the gastric epithelium activates cellular bicarbonate secretion via SLC26A9 Cl(-)/HCO(3)(-). | |
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MedLine Citation:
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PMID: 20413716 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Gastric surface pH (pH(o)) transiently increases in response to focal epithelial damage. The sources of that increase, either from paracellular leakage of interstitial fluid or transcellular acid/base fluxes, have not been determined. Using in vivo microscopy approaches we measured pH(o) with Cl-NERF, tissue permeability with intravenous fluorescent-dextrans to label interstitial fluid (paracellular leakage), and gastric epithelial intracellular pH (pH(i)) with SNARF-5F (cellular acid/base fluxes). In response to two-photon photodamage, we found that cell-impermeant dyes entered damaged cells from luminal or tissue compartments, suggesting a possible slow transcellular, but not paracellular, route for increased permeability after damage. Regarding cytosolic acid/base status, we found that damaged cells acidified (6.63 +/- 0.03) after photodamage, compared with healthy surface cells both near (7.12 +/- 0.06) and far (7.07 +/- 0.04) from damage (P < 0.05). This damaged cell acidification was further attenuated with 20 muM intravenous EIPA (6.34 +/- 0.05, P < 0.05) but unchanged by addition of 0.5 mM luminal H(2)DIDS (6.64 +/- 0.08, P > 0.05). Raising luminal pH did not realkalinize damaged cells, suggesting that the mechanism of acidification is not attributable to leakiness to luminal protons. Inhibition of apical HCO(3)(-) secretion with 0.5 mM luminal H(2)DIDS or genetic deletion of the solute-like carrier 26A9 (SLC26A9) Cl(-)/HCO(3)(-) exchanger blocked the pH(o) increase normally observed in control animals but did not compromise repair of damaged tissue. Addition of exogenous PGE(2) significantly increased pH(o) in wild-type, but not SLC26A9 knockout, animals, suggesting that prostaglandin-stimulated HCO(3)(-) secretion is fully mediated by SLC26A9. We conclude that cellular HCO(3)(-) secretion, likely through SLC26A9, is the dominant mechanism whereby surface pH transiently increases in response to photodamage. |
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Authors:
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Elise S Demitrack; Manoocher Soleimani; Marshall H Montrose |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural Date: 2010-04-22 |
Journal Detail:
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Title: American journal of physiology. Gastrointestinal and liver physiology Volume: 299 ISSN: 1522-1547 ISO Abbreviation: Am. J. Physiol. Gastrointest. Liver Physiol. Publication Date: 2010 Jul |
Date Detail:
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Created Date: 2010-06-16 Completed Date: 2010-07-12 Revised Date: 2013-05-29 |
Medline Journal Info:
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Nlm Unique ID: 100901227 Medline TA: Am J Physiol Gastrointest Liver Physiol Country: United States |
Other Details:
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Languages: eng Pagination: G255-64 Citation Subset: IM |
Affiliation:
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Department of Molecular & Cellular Physiology, University of Cincinnati, 231 Albert Sabin Way, Cincinnati, OH 45267, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Antiporters / deficiency, genetics, metabolism* Bicarbonates / metabolism* Biological Transport Chlorides / metabolism* Cyclic AMP / analogs & derivatives, metabolism Dextrans / metabolism Dinoprostone / metabolism Fluoresceins / metabolism Gastric Acid / metabolism* Gastric Acidity Determination Gastric Mucosa / drug effects, metabolism*, pathology, radiation effects Hydrogen-Ion Concentration Mice Mice, Inbred C57BL Mice, Knockout Microscopy, Confocal Microscopy, Fluorescence, Multiphoton NADP / metabolism Permeability Time Factors |
| Grant Support | |
ID/Acronym/Agency:
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DK 62809/DK/NIDDK NIH HHS; R01 DK 54940/DK/NIDDK NIH HHS; R01 DK054940-10/DK/NIDDK NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Antiporters; 0/Bicarbonates; 0/Chlorides; 0/Fluoresceins; 0/Slc26a9 protein, mouse; 0/fluorescein-dextran; 363-24-6/Dinoprostone; 39824-30-1/8-aminohexylamino cAMP; 53-59-8/NADP; 60-92-4/Cyclic AMP; 9004-54-0/Dextrans |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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