Role of caspase-3/E-cadherin in helicobacter pylori-induced apoptosis of gastric epithelial cells

// Yongmei Yang 1, 2 , Jie Du 1 , Fen Liu 3 , Xiaoyan Wang 3 , Xiaohui Li 1 and Yuanjian Li 1 1 Department of Pharmacology, Xiangya School of Pharmaceutical Science, Central South University, Changsha, China 2 Department of Anatomy, School of Medicine, University of South China, Hengyang, China 3 Department of Gastroenterology, Third Xiangya Hospital, Central South University, Changsha, China Correspondence to: Yuanjian Li, email: yuan_jianli@sina.com Xiaohui Li, email: xiaohuili@csu.edu.cn 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 ABSTRACT 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 .