Bax translocation and mitochondrial fragmentation induced by Helicobacter pylori.

摘要: Background and aims: Previous in vitro vivo studies have revealed an association between Helicobacter pylori infection apoptosis gastric epithelial cells. Although involvement of the Bcl-2 family proteins as well cytochrome c release has been demonstrated H induced cell death, exact role mitochondria during this type programmed death not fully elucidated. Therefore, we sought to determine whether or Bax translocation mitochondrial fragmentation occur on exposure cells pylori, resulting death. Methods: Experiments were performed with human adenocarcinoma (AGS) cells, AGS transfected HPV-E6 gene (which inactivates p53 function), AGS-neo (transfected backbone construct), mouse embryonic fibroblasts (MEFs), p19ARF null (ARF−/−) MEFs. Cells incubated a cag positive strain for up 24 hours, lysed, cytoplasmic membrane fractions analysed by western blot translocation. Results: was detected AGS, AGS-neo, normal MEF after three but ARF−/− MEFs Translocation incubation also AGS-E6 (inactive gene) lesser degree than In parallel studies, morphology living infected assessed confocal microscopy. Mitochondrial detectable 10 hours seven wild-type MEFs, significantly increased comparison ARF (43% v 10.4%, respectively). Furthermore, depolarisation caspase-3 activity initiated within four these events inhibited forced expression Bcl-2. Conclusions: These data suggest that apoptosis, translocates which subsequently undergo profound fragmentation. Functional may play important modification.