Abstract
In our previous study, γ-glutamyl transpeptidase (GGT) isolated from Helicobacter pylori induced apoptosis of AGS cells. Here, we investigate Ca(2+) effects on GGT-induced apoptosis. The GGT transiently and significantly increased intracellular Ca(2+) concentration ([Ca(2+)]i) in AGS cells in a dose-dependent manner (P < 0.05). The GGT-induced Ca(2+) increase resulted from Ca(2+) influx and release through the phospholipase C - inositol 1,4,5-trisphosphate (PLC-IP3) pathway. The GGT-induced apoptosis was significantly reduced by treatment with U73122 (a PLC inhibitor) and xestospongin (an IP3 receptor antagonist) (P < 0.05). These results indicate that GGT could induce apoptosis of AGS cells by high levels of [Ca(2+)]i.
Keywords:
Helicobacter pylori; apoptose; apoptosis; calcium; γ-glutamyl transpeptidase.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Apoptosis*
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Calcium / metabolism*
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Cell Line, Tumor
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Enzyme Inhibitors / pharmacology
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Estrenes / pharmacology
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Helicobacter pylori / metabolism*
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Humans
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Inositol 1,4,5-Trisphosphate Receptors / antagonists & inhibitors
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Inositol 1,4,5-Trisphosphate Receptors / metabolism*
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Macrocyclic Compounds / pharmacology
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Oxazoles / pharmacology
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Pyrrolidinones / pharmacology
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Recombinant Proteins / metabolism
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Type C Phospholipases / antagonists & inhibitors
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Type C Phospholipases / metabolism*
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gamma-Glutamyltransferase / genetics
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gamma-Glutamyltransferase / metabolism*
Substances
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Enzyme Inhibitors
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Estrenes
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Inositol 1,4,5-Trisphosphate Receptors
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Macrocyclic Compounds
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Oxazoles
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Pyrrolidinones
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Recombinant Proteins
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xestospongin C
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1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione
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gamma-Glutamyltransferase
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Type C Phospholipases
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Calcium