Helicobacter pylori γ-glutamyl transpeptidase-induced Ca2+ release via PLC–IP3 receptors in AGS cells-Reference-Cited by-同舟云学术

Helicobacter pylori γ-glutamyl transpeptidase-induced Ca2+ release via PLC–IP3 receptors in AGS cells

Published:2014-12 Issue:12 Volume:60 Page:865-868
ISSN:0008-4166
Container-title:Canadian Journal of Microbiology
language:en
Short-container-title:Can. J. Microbiol.

Author:

Park Eun-Hee¹,Kim Jung-Min¹,Kim Kyung-Mi¹,Kang Dawon²,Cho Young-Ah¹,Choi Jun-Young³,Song Jea-Young¹,Kang Hyung-Lyun¹⁴,Lee Woo-Kon¹⁴,Cho Myung-Je¹⁴,Rhee Kwang-Ho¹⁴,Seo Ji-Hyun⁵,Youn Hee-Shang⁵,Baik Seung-Chul¹⁴

Affiliation:

1. Department of Microbiology, Gyeongsang National University School of Medicine, Chiram-dong 90, Jinju 660-751, Korea.

2. Department of Physiology, Gyeongsang National University School of Medicine, Jinju 660-751, Korea.

3. Department of Thoracic and Cardiovascular Surgery, Gyeongsang National University School of Medicine, Jinju 660-751, Korea.

4. Research Institute of Life Science, Gyeongsang National University, Jinju 660-751, Korea.

5. Department of Pediatrics, Gyeongsang National University, School of Medicine, Gyeongsang Institute of Health Science, Jinju 660-751, Korea.

Abstract

In our previous study, γ-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.

Publisher

Canadian Science Publishing

Subject

Genetics,Molecular Biology,Applied Microbiology and Biotechnology,General Medicine,Immunology,Microbiology

Link

http://www.nrcresearchpress.com/doi/pdf/10.1139/cjm-2014-0464

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