Document Detail


Inhibition of small-conductance Cl- channels by the interleukin-1beta-stimulated production of superoxide in rabbit gastric parietal cells.
MedLine Citation:
PMID:  12815175     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
We have shown previously that the G protein-coupled production of superoxide anion (O2-) leads to closure of small-conductance Cl- channels (0.3-0.4 pS) in the basolateral membrane of rabbit parietal cells. In the present study, effects of interleukin-1beta (IL-1beta) on the Cl- channel were investigated. In the whole-cell patch-clamp recording, IL-1beta (0.3-10 ng ml-1) inhibited the whole-cell Cl- current recorded from a parietal cell within isolated rabbit gastric glands. Variance noise analysis of the whole-cell Cl- current showed that the single channel conductance of the Cl- channel that is sensitive to IL-1beta is 0.37 pS. The IL-1beta (1 ng ml-1)-induced decrease of the Cl- current was abolished by anti-IL-1beta antibody (2 microg ml-1), recombinant IL-1 receptor antagonist (500 ng ml-1), GDPbetaS (500 microM) and superoxide dismutase (100 units ml-1), a scavenger of O2-. Northern blot analysis showed that the mRNA of the IL-1 receptor was selectively expressed in rabbit gastric parietal cells. In the dihydrofluorescein diacetate-loaded single parietal cells in gastric glands, IL-1beta (0.3-10 ng ml-1) stimulated the production of oxygen radicals. Y-27632 (1-10 microM), a specific Rho-kinase inhibitor, and fluvastatin (10 microM), an indirect inhibitor for Rho proteins, significantly inhibited the IL-1beta-induced effects on the channel activity and production of oxygen radicals. IL-1beta (0.3-10 ng ml-1) activated Rho in the parietal cells. These results indicate that IL-1beta binds to the IL-1 receptor of gastric parietal cells and inhibits the small-conductance Cl- channel via the G protein-mediated Rho/Rho-kinase-dependent production of O2-.
Authors:
Hideki Sakai; Yuta Ohira; Akiko Tanaka; Tomoyuki Suzuki; Akira Ikari; Magotoshi Morii; Noriaki Takeguchi
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2003-06-18
Journal Detail:
Title:  The Journal of physiology     Volume:  551     ISSN:  0022-3751     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  2003 Aug 
Date Detail:
Created Date:  2003-08-18     Completed Date:  2004-04-21     Revised Date:  2013-06-09    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  207-17     Citation Subset:  IM    
Affiliation:
Department of Pharmaceutical Physiology, Faculty of Pharmaceutical Sciences, Toyama Medical and Pharmaceutical University, 2630 Sugitani, Toyama 930-0194, Japan. sakaih@ms.toyama-mpu.ac.jp
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MeSH Terms
Descriptor/Qualifier:
Acute-Phase Proteins / drug effects,  physiology
Animals
Chloride Channels / antagonists & inhibitors*,  physiology
Electric Conductivity
GTP-Binding Proteins / physiology
Interleukin-1 / pharmacology*
Intracellular Membranes / metabolism
Intracellular Signaling Peptides and Proteins
Parietal Cells, Gastric / drug effects,  metabolism*
Protein-Serine-Threonine Kinases / physiology
Rabbits
Reactive Oxygen Species / metabolism
Superoxides / metabolism*
rho-Associated Kinases
Chemical
Reg. No./Substance:
0/Acute-Phase Proteins; 0/Chloride Channels; 0/Interleukin-1; 0/Intracellular Signaling Peptides and Proteins; 0/Reactive Oxygen Species; 0/acute-phase protein rho; 11062-77-4/Superoxides; EC 2.7.11.1/Protein-Serine-Threonine Kinases; EC 2.7.11.1/rho-Associated Kinases; EC 3.6.1.-/GTP-Binding Proteins
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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