Role of caspase-3/E-cadherin in helicobacter pylori-induced apoptosis of gastric epithelial cells
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Yongmei Yang1,2, Jie Du1, Fen Liu3, Xiaoyan Wang3, Xiaohui Li1 and Yuanjian Li1
1Department of Pharmacology, Xiangya School of Pharmaceutical Science, Central South University, Changsha, China
2Department of Anatomy, School of Medicine, University of South China, Hengyang, China
3Department of Gastroenterology, Third Xiangya Hospital, Central South University, Changsha, China
Yuanjian Li, email: firstname.lastname@example.org
Xiaohui Li, email: email@example.com
Keywords: helicobacter pylori, caspase-3, E-cadherin, E-cadherin/carboxy-terminal fragment 3 (E-cad/CTF3), apoptosis
Received: January 04, 2017 Accepted: June 20, 2017 Published: July 22, 2017
This study was designed to investigate the role of caspase-3/E-cadherin in Helicobacter pylori (H. pylori) -induced gastric epithelial apoptosis in cells, animal models and clinical gastritis patients. In cultured gastric mucosal epithelial cells, gastric glandular epithelial cells and C57BL/6 mice, H. pylori infection significantly induced apoptosis of gastric epithelial cells, down-regulated full-length E-cadherin and Bcl-2 expression, and up-regulated cleaved-caspase-3, E-cadherin/carboxy-terminal fragment 3 and Bax expression. Z-DEVD-FMK, an inhibitor of caspase-3, attenuated the effect of H. pylori. E-cadherin overexpression significantly inhibited the apoptosis of GES-1 and SGC-7901 cells induced by the H. pylori. The results from clinical studies also showed down-regulation of E-cadherin, up-regulation of cleaved-caspase-3 expression and increased apoptosis in gastric tissues from gastritis patients with H. pylori infection. These results suggest that the caspase-3/E-cadherin pathway is involved in the apoptosis of gastric epithelial cells induced by H. pylori.
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