Abstract
BackgroundH. pylori infection significantly attenuated the expression of HSP70 in gastric mucosal cells. However, the role of HSP70 cancellation in H. pylori-associated cell damages is largely unclear.MethodsSmall interfering RNA (siRNA) was used to down-regulate HSP70 in gastric epithelial cell lines AGS. The transfected cells were then incubated with H. pylori and the functions of HSP70 suppression were observed by viability assay, cell cycle analyses and TUNEL assay. HSP70 target apoptotic proteins were further identified by Western blot.ResultsThe inhibition of HSP70 has further increased the effect of growth arrest and apoptosis activation triggered by H. pylori in gastric epithelial cells. The anti-proliferation function of HSP70 depletion was at least by up-regulating p21 and cell cycle modulation with S-phase accumulation. An increase of apoptosis-inducing factor (AIF) and cytosolic cytochrome C contributes to the activation of apoptosis following down-regulation of intracellular HSP70. Extracellular HSP70 increased cellular resistance to apoptosis by suppression the release of AIF and cytochrome c from mitochondria, as well as inhibition of p21 expression.ConclusionsThe inhibition of HSP70 aggravated gastric cellular damages induced by H. pylori. Induction of HSP70 could be a potential therapeutic target for protection gastric mucosa from H. pylori-associated injury.
Highlights
H. pylori infection significantly attenuated the expression of HSP70 in gastric mucosal cells
H. pylori infection suppressed HSP70 expression in gastric cell line AGS cells We first examined the influence of H. pylori on HSP70 expression in AGS cells
Basal HSP70 expression was found relatively high in the gastric epithelial cells, but H. pylori infection induced a significant suppression of HSP70
Summary
H. pylori infection significantly attenuated the expression of HSP70 in gastric mucosal cells. Helicobacter pylori (H. pylori) infection leads to significant inflammations in the gastric mucosa, which is closely associated with development of atrophic gastritis, peptic ulcer, gastric cancer, and mucosa-associated lymphoid tissue (MALT) lymphoma. Animal studies have demonstrated that H. pylori infection damages gastric mucosa by either disrupting the balance in cell apoptosis. Our previous animal studies have introduced ammonia solution to simulate the conditions of H. pylori infection, and succeeded in inducing atrophic gastritis in rats [12]. Further studies demonstrated that induction of HSP70 expression is beneficial for preventing gastric atrophy and maintaining mucosal functions in gastric cells [12]. We investigated the correlation of HSP70 inhibition with the mucosal damages induced by H. pylori in this study
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
