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 var 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.
Obst
Barbara
B
Department of Pharmacology, Hannover Medical School, D-30625 Hannover, Germany.
Schütz
Silke
S
Ledig
Susanne
S
Wagner
Siegfried
S
Beil
Winfried
W
D017209:Apoptosis; D053148:Caspase 3; D053453:Caspase 9; D020169:Caspases / Q000378:metabolism; D002453:Cell Cycle; D005753:Gastric Mucosa; D016480:Helicobacter pylori / Q000472:pathogenicity*; D007527:Isoenzymes / Q000502:physiology; D011493:Protein Kinase C / Q000502:physiology*; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology; D014407:Tumor Cells, Cultured
D007527:Isoenzymes; D011493:Protein Kinase C; D053148:Caspase 3; D053453:Caspase 9; D020169:Caspases; D013755:Tetradecanoylphorbol Acetate