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  • Title: Helicobacter pylori fatty acid cis 9,10-methyleneoctadecanoic acid increases [Ca2+]i, activates protein kinase C and stimulates acid secretion in parietal cells.
    Author: Beil W, Birkholz C, Wagner S, Sewing KF.
    Journal: Prostaglandins Leukot Essent Fatty Acids; 1998 Aug; 59(2):119-25. PubMed ID: 9774175.
    Abstract:
    The effect of the Helicobacter pylori (H. pylori) fatty acid cis 9,10-methyleneoctadecanoic acid (MOA) on gastric acid secretion was studied in isolated guinea-pig parietal cells. MOA (1 and 3 micromol/l) stimulated basal and enhanced histamine- and dibutyryl cyclic AMP-stimulated acid secretion in parietal cells. MOA increased intracellular free [Ca2+]i concentration in a concentration-dependent manner. The source of [Ca2+]i was extracellular as demonstrated by depletion of [Ca2+]i with EGTA. Furthermore, MOA caused activation of parietal cell protein kinase C (PKC). The effect of MOA upon PKC activation was [Ca2+]i-dependent but did not require phosphatidylserine as phospholipid co-factor. Similarly to the effect of diolein, MOA increased the stimulatory effect of phosphatidylserine at low [Ca2+]i concentrations. Treatment of parietal cells with MOA caused translocation of PKC from the cytosol to the membrane-associated cell fraction. We propose that MOA stimulates parietal cell acid secretion presumably by an increase of cytosolic free [Ca2+]i concentrations and PKC activation.
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