title: [The effect of rosiglitazone on the cell proliferation and the expressions of p27 and skp2 in helicobacter pylori infected human gastric epithelial cells].
abstract: OBJECTIVE
  Ligands for peroxisome proliferator-activated receptorgamma (PPARgamma), a member of the ligand-activated nuclear receptor superfamily, exhibit anti-tumoral effects and are associated with de novo synthesis of proteins involved in regulating the cell cycle and cell survival/death. Helicobacter pylori (H. pylori) is an etiologic agent for gastric adenocarcinoma, and raises the cell turnover of gastric epithelium. The aim of this study was to investigate the effect of PPARgamma ligand rosiglitazone on the cell proliferation and the expressions of p27 and Skp2 protein in H. pylori infected gastric epithelial cells.
  
  
  METHODS
  We examined the expression of PPARgamma by Western blot in H. pylori infected AGS human gastric epithelial cells. The effect of rosiglitazone on the survival of H. pylori infected AGS cells was assessed by cell viability assay. After the treatment of rosiglitazone in H. pylori infected AGS cells, the expressions of p27 and Skp2 were assessed by Western blot.
  
  
  RESULTS
  The expression of PPARgamma protein was increased in H. pylori infected AGS cells. Cell growth was inhibited and decreased in dose- and time- dependent manner in H. pylori infected AGS cells treated with rosiglitazone. A decrease in Skp2 expression and a reciprocal increase in p27 expression were found in dose- and time-dependent manner in H. pylori infected AGS cells treated with rosiglitazone.
  
  
  CONCLUSIONS
  Rosiglitazone inhibited the growth of H. pylori infected AGS cells. Rosiglitazone attenuated Skp2 expression, thereby promoting p27 accumulation in H. pylori infected human gastric epithelial cells. Further studies will be needed to find the effects of accumulation on cell turnover in H. pylori infection and the role in the H. pylori-associated gastric carcinogenesis.
authors.affiliation: Departments of Internal Medicine, The Catholic University of Korea College of Medicine, Seoul, Korea.
authors.forename: Sung Soo
authors.initials: SS
authors.lastname: Kim
authors.forename: Young Seok
authors.initials: YS
authors.lastname: Cho
authors.forename: Hyung Keun
authors.initials: HK
authors.lastname: Kim
authors.forename: Ok Ran
authors.initials: OR
authors.lastname: Shin
authors.forename: Hiun Suk
authors.initials: HS
authors.lastname: Chae
authors.forename: Myung Gyu
authors.initials: MG
authors.lastname: Choi
authors.forename: In Sik
authors.initials: IS
authors.lastname: Chung
mesh_terms: D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D002460:Cell Line; D049109:Cell Proliferation; D050760:Cyclin-Dependent Kinase Inhibitor p27 / Q000378:metabolism*; D004847:Epithelial Cells / Q000378:metabolism / Q000382:microbiology*; D005753:Gastric Mucosa / Q000166:cytology / Q000378:metabolism / Q000382:microbiology*; D016480:Helicobacter pylori; D006801:Humans; D047495:PPAR gamma / Q000037:antagonists & inhibitors / Q000378:metabolism; D000077154:Rosiglitazone; D044786:S-Phase Kinase-Associated Proteins / Q000378:metabolism*; D045162:Thiazolidinediones / Q000494:pharmacology*
chemical_list: D000900:Anti-Bacterial Agents; D047495:PPAR gamma; D044786:S-Phase Kinase-Associated Proteins; D045162:Thiazolidinediones; D000077154:Rosiglitazone; D050760:Cyclin-Dependent Kinase Inhibitor p27