title: Effects of H pylori infection on gap-junctional intercellular communication and proliferation of gastric epithelial cells in vitro.
abstract: OBJECTIVE
  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).
  
  
  CONCLUSIONS
  Compared with CagA(-) H pylori strains, CagA(+) strains down-regulate GJIC of gastric epithelial 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.
authors: Central Laboratory, Children's Hospital, School of Medicine, Zhejiang University, 57 Zhugan Lane, Hangzhou 310003, Zhejiang Province, China. rtao1211@yahoo.com.cn
authors: Ran
authors: R
authors: Tao
authors: Miao-Feng
authors: MF
authors: Hu
authors: Jin-Tu
authors: JT
authors: Lou
authors: Yong-Liang
authors: YL
authors: Lei
mesh_terms: D000942:Antigens, Bacterial / Q000032:analysis; D001426:Bacterial Proteins / Q000032:analysis; D002450:Cell Communication; D002460:Cell Line; D049109:Cell Proliferation; D004847:Epithelial Cells / Q000382:microbiology* / Q000473:pathology; D036681:Fluorescence Recovery After Photobleaching; D017629:Gap Junctions / Q000382:microbiology* / Q000473:pathology; D005753:Gastric Mucosa / Q000382:microbiology* / Q000473:pathology; D016481:Helicobacter Infections / Q000382:microbiology* / Q000473:pathology; D016480:Helicobacter pylori / Q000737:chemistry / Q000472:pathogenicity*; D006801:Humans
chemical_list: D000942:Antigens, Bacterial; D001426:Bacterial Proteins; C080866:cagA protein, Helicobacter pylori