ArticleThe Journal of physiology2003
Inhibition of small-conductance Cl- channels by the interleukin-1beta-stimulated production of superoxide in rabbit gastric parietal cells.
Article in The Journal of physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed, 7 citations in OpenAlex.
- Cyclic AMP-dependent Cl- secretion induced by thromboxane A2 in isolated human colon.The Journal of physiology · 2005Article
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7 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
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-.
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