title: Helicobacter pylori γ-glutamyl transpeptidase-induced Ca(2+) release via PLC-IP3 receptors in AGS cells.
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.
authors.affiliation: a Department of Microbiology, Gyeongsang National University School of Medicine, Chiram-dong 90, Jinju 660-751, Korea.
authors.forename: Eun-Hee
authors.initials: EH
authors.lastname: Park
authors.forename: Jung-Min
authors.initials: JM
authors.lastname: Kim
authors.forename: Kyung-Mi
authors.initials: KM
authors.lastname: Kim
authors.forename: Dawon
authors.initials: D
authors.lastname: Kang
authors.forename: Young-Ah
authors.initials: YA
authors.lastname: Cho
authors.forename: Jun-Young
authors.initials: JY
authors.lastname: Choi
authors.forename: Jea-Young
authors.initials: JY
authors.lastname: Song
authors.forename: Hyung-Lyun
authors.initials: HL
authors.lastname: Kang
authors.forename: Woo-Kon
authors.initials: WK
authors.lastname: Lee
authors.forename: Myung-Je
authors.initials: MJ
authors.lastname: Cho
authors.forename: Kwang-Ho
authors.initials: KH
authors.lastname: Rhee
authors.forename: Ji-Hyun
authors.initials: JH
authors.lastname: Seo
authors.forename: Hee-Shang
authors.initials: HS
authors.lastname: Youn
authors.forename: Seung-Chul
authors.initials: SC
authors.lastname: Baik
mesh_terms: D017209:Apoptosis; D002118:Calcium / Q000378:metabolism*; D045744:Cell Line, Tumor; D004791:Enzyme Inhibitors / Q000494:pharmacology; D004963:Estrenes / Q000494:pharmacology; D016480:Helicobacter pylori / Q000378:metabolism*; D006801:Humans; D053496:Inositol 1,4,5-Trisphosphate Receptors / Q000037:antagonists & inhibitors / Q000378:metabolism*; D047028:Macrocyclic Compounds / Q000494:pharmacology; D010080:Oxazoles / Q000494:pharmacology; D011760:Pyrrolidinones / Q000494:pharmacology; D011994:Recombinant Proteins / Q000378:metabolism; D010738:Type C Phospholipases / Q000037:antagonists & inhibitors / Q000378:metabolism*; D005723:gamma-Glutamyltransferase / Q000235:genetics / Q000378:metabolism*
chemical_list: D004791:Enzyme Inhibitors; D004963:Estrenes; D053496:Inositol 1,4,5-Trisphosphate Receptors; D047028:Macrocyclic Compounds; D010080:Oxazoles; D011760:Pyrrolidinones; D011994:Recombinant Proteins; C511704:xestospongin C; C060229:1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione; D005723:gamma-Glutamyltransferase; D010738:Type C Phospholipases; D002118:Calcium
keywords: Helicobacter pylori; apoptose; apoptosis; calcium; γ-glutamyl transpeptidase