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Helicobacter pylori gamma-glutamyl transpeptidase-induced Ca2+ release via PLC-IP3 receptors in AGS cells
- Authors
- Park, Eun-Hee; Kim, Jung-Min; Kim, Kyung-Mi; Kang, Dawon; Cho, Young-Ah; Choi, Jun-Young; Song, Jea-Young; Kang, Hyung-Lyun; Lee, Woo-Kon; Cho, Myung-Je; Rhee, Kwang-Ho; Seo, Ji-Hyun; Youn, Hee-Shang; Baik, Seung-Chul
- Issue Date
- Dec-2014
- Publisher
- CANADIAN SCIENCE PUBLISHING, NRC RESEARCH PRESS
- Keywords
- apoptosis; calcium; gamma-glutamyl transpeptidase; Helicobacter pylori
- Citation
- CANADIAN JOURNAL OF MICROBIOLOGY, v.60, no.12, pp 865 - 868
- Pages
- 4
- Indexed
- SCI
SCIE
SCOPUS
- Journal Title
- CANADIAN JOURNAL OF MICROBIOLOGY
- Volume
- 60
- Number
- 12
- Start Page
- 865
- End Page
- 868
- ISSN
- 0008-4166
1480-3275
- Abstract
- In our previous study, gamma-glutamyl transpeptidase (GGT) isolated from Helicobacter pylori induced apoptosis of AGS cells. Here, we investigate Ca2+ effects on GGT-induced apoptosis. The GGT transiently and significantly increased intracellular Ca2+ concentration ([Ca2+](i)) in AGS cells in a dose-dependent manner (P < 0.05). The GGT-induced Ca2+ increase resulted from Ca2+ 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 [Ca2+](i).
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