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.
Highlights
Peptic ulcer is characterized by the formation of chronic gastric ulcer or duodenal mucosa ulcer, and the prevalence varies from 11% to 69% in different countries [1]
H. pylori-induced gastric epithelial cell apoptosis is a major mechanism for gastric mucosal damage. in vitro and in vivo experiments showed that H. pylori and the secretion of cytotoxins, such as cytotoxin-associated protein A (CagA), vacuolating cytotoxin A (VacA), lipopolysaccharide, and others, could induce gastric epithelial cell apoptosis and gastric ulcer formation [3, 4]
H. pylori infection plays a critical role in the pathogenesis of chronic gastritis and gastric ulcer diseases, and gastric epithelial apoptosis is an important pathophysiological hallmark of gastric mucosal injury [22, 23]
Summary
Peptic ulcer is characterized by the formation of chronic gastric ulcer or duodenal mucosa ulcer, and the prevalence varies from 11% to 69% in different countries [1]. Peptic ulcer can be complicated by bleeding, perforation, pyloric obstruction and inducing cancer. The incidence of this disease involves a variety of factors, such as dietary, chemical (smoking, alcohol and drugs), biological (Helicobacter pylori, H. pylori), mental and environmental factors. The mechanism of H. pylori-induced gastric mucosal injury has not been fully elucidated. H. pylori-induced gastric epithelial cell apoptosis is a major mechanism for gastric mucosal damage. In vitro and in vivo experiments showed that H. pylori and the secretion of cytotoxins, such as cytotoxin-associated protein A (CagA), vacuolating cytotoxin A (VacA), lipopolysaccharide, and others, could induce gastric epithelial cell apoptosis and gastric ulcer formation [3, 4]. Caspase-3 induces apoptosis by cleaving specific substrates, which has been documented by the generation of caspase-3 cleaved substrates, accompanied by morphological and molecular characteristics of apoptosis [10, 11]
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