The Helicobacter pylori fatty acid cis-9,10-methyleneoctadecanoic acid stimulates protein kinase C and increases DNA synthesis of gastric HM02 cells

Protein kinase C (PKC) has been implicated in the control of epithelial pro liferative activity and in the process of malignant transformation. Helicob acter pylori (H.p.) infection is associated with increased gastric epitheli al cell proliferation and has been linked with gastric carcinoma. In the pr esent study, we report that the H.p. fatty acid cis-9,10-methyleneoctadecan oic acid (MOA) directly activates PKC (K-a 3.3 mu M). The effect of MOA upo n PKC activation was Ca2+ dependent but did not require phosphatidylserine as phospholipid cofactor. MOA increased the stimulatory effect of phosphati dylserine at low Ca2+ (1 mu M) concentrations. These findings indicate that MOA interacts at the phospholipid- and the diacylglycerol-binding domain t o elicit PKC activation. Treatment of gastric mucous cells HM02 caused tran slocation of PKC from the cytosol to the nuclear, mitochondrial and membran e fraction. Furthermore. MOA stimulated [H-3]thymidine incorporation into t he DNA of HM02 cells. Our results show that the H.p, fatty acid MOA activat es PKC and increases DNA synthesis in gastric epithelial cells.