Helicobacter pylori-induced apoptosis in gastric epithelial cells is blocked by protein kinase C activation

Apoptosis plays a major role in gastrointestinal epithelial cell turnover. We have examined induction of apoptosis by Helicobacter pylori in gastric AGS cells and the role of protein kinase C (PKC) which has been shown to modulate programmed cell death. Incubation of AGS cells with H. pylori resulted in an activation of caspases 3 and 9 and induced programmed cell death. The PKC activator 12-O-tetradecanoylphorbol-13-acetate (TPA) caused translocation of PKC gamma, delta and epsilon, prevented H. pylori-induced caspase activation and programmed cell death. Cocultivation of AGS cells with H. pylori resulted in a translocation of the atypical PKC isoform PKC lambda. We suggest that inhibition of H. pylori induced apoptosis by PKC activation can play a role in the process of neoplastic transformation. (C) 2002 Elsevier Science Ltd. All rights reserved.