The Effect of Rosiglitazone on the Cell Proliferation and the Expressions of p27 and Skp2 in Helicobacter pylori Infected Human Gastric Epithelial Cells.
10.4166/kjg.2010.55.4.225
- Author:
Sung Soo KIM
1
;
Young Seok CHO
;
Hyung Keun KIM
;
Ok Ran SHIN
;
Hiun Suk CHAE
;
Myung Gyu CHOI
;
In Sik CHUNG
Author Information
1. Department of Internal Medicine, The Catholic University of Korea College of Medicine, Seoul, Korea. yscho@catholic.ac.kr
- Publication Type:Original Article ; English Abstract
- Keywords:
Helicobacter pylori;
Peroxisome proliferator-activated receptor gamma;
p27;
S-Phase kinase-associated proteins
- MeSH:
Anti-Bacterial Agents/*pharmacology;
Cell Line;
Cell Proliferation;
Cyclin-Dependent Kinase Inhibitor p27/*metabolism;
Epithelial Cells/metabolism/*microbiology;
Gastric Mucosa/cytology/metabolism/*microbiology;
*Helicobacter pylori;
Humans;
PPAR gamma/antagonists &inhibitors/metabolism;
S-Phase Kinase-Associated Proteins/*metabolism;
Thiazolidinediones/*pharmacology
- From:The Korean Journal of Gastroenterology
2010;55(4):225-231
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND/AIMS: Ligands for peroxisome proliferator-activated receptor gamma (PPAR gamma), 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 PPAR gamma 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 PPAR gamma 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 PPAR gamma 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.
