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AIM: To explore the effects of H pylori infection on gap-junctional intercellular communication (GJIC) and proliferation of gastric epithelial cells in vitro. METHODS: A human gastric epithelial cell line (SGC-7901) cultured on coverslips was exposed overnight to intact H pylori (CagA+ or CagA-strains) and sonicated extracts,respectively. GJIC between the cells was detected by fluorescence redistribution after photobleaching (FRAP) technique. Proliferation of SGC cells was determined by methylthiazolyl tetrazolium (MTT) assay. RESULTS: When compared with control in which cells were cultured with simple medium alone,both CagA+ and CagA-H pylori isolates could inhibit GJIC (CagA+: F = 57.98,P < 0.01; CagA-: F = 29.59,P < 0.01) and proliferation (CagA+: F = 42.65,P < 0.01; CagA-: F = 58.14,P < 0.01) of SGC-7901 cells. Compared with CagA-strains,CagA+ H pylori more significantly down-regulated GJIC of gastric cells (intact H pylori: t = 13.86,P < 0.01; sonicated extracts: t = 11.87,P < 0.01) and inhibited proliferation gastric cells to a lesser extent in vitro (intact H pylori: t = 3.06,P < 0.05; sonicated extracts: t = 3.94,P < 0.01). CONCLUSION: Compared with CagA-H pylori strains,CagA+ strains down-regulate GJIC of gastric epithelia cells more significantly and inhibit proliferation of gastric cells to a lesser extent in vitro . H pylori ,especially CagA+ strains,may play an important role in gastric carcinogenesis.
AIM: To explore the effects of H pylori infection on gap-junctional intercellular communication (GJIC) and proliferation of gastric epithelial cells in vitro. METHODS: A human gastric epithelial cell line (SGC- 7901) cultured on coverslips was exposed overnight to intact H GJIC between the cells was detected by fluorescence redistribution after photobleaching (FRAP) technique. Proliferation of SGC cells was determined by methylthiazolyl tetrazolium (MTT) assay. RESULTS: When compared with control (CagA + or CagA-strain) and sonicated extracts, CagA-: F = 29.59, P <0.01) and proliferation (CagA +: F = Compared with CagA-strain, CagA + H pylori more significantly down-regulated GJIC of gastric cells (intact H pylori: t = 13.86, P <0.01) P <0.01; sonicated extracts: t = 11.87, P <0.0 1), and inhibited proliferation of gastric cells to a lesser extent in vitro. CONCLUSION: Compared with CagA-H pylori strain, CagA + strain (with intact H pylori: t = 3.06, P < down-regulate GJIC of gastric epithelia cells more significantly and inhibited proliferation of gastric cells to a lesser extent in vitro. H pylori, especially CagA +, may play an important role in gastric carcinogenesis.