Expression of Peroxisome Proliferator-activated Receptor (PPAR)gamma in Helicobacter pylori-infected Gastric Epithelium.
- Author:
Seong Hyun SON
1
;
Hyung Keun KIM
;
Jeong Seon JI
;
Young Seok CHO
;
Sung Soo KIM
;
Hiun Suk CHAE
;
Myung Gyu CHOI
;
Sok Won HAN
;
Kyu Yong CHOI
;
In Sik CHUNG
;
Ok Ran SHIN
Author Information
1. Departments 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
- MeSH:
Adult;
Colonic Neoplasms/metabolism/microbiology/pathology;
Computer Systems;
Female;
Gastric Mucosa/*metabolism/microbiology/pathology;
Gastritis/*metabolism/microbiology/pathology;
Helicobacter Infections/*metabolism/microbiology;
*Helicobacter pylori;
Humans;
Immunohistochemistry;
Male;
Middle Aged;
PPAR gamma/*metabolism;
Reverse Transcriptase Polymerase Chain Reaction;
Stomach Neoplasms/metabolism/microbiology/pathology
- From:The Korean Journal of Gastroenterology
2007;49(2):72-78
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND/AIMS: Peroxisome proliferator-activated receptorgamma (PPARgamma), a nuclear transcription factor, plays a critical role in the regulation of gene expression associated with inflammation and cancer. PPARgamma is expressed in human gastric cancer as well as in colon cancer. Activation of PPARgamma by ligand produces pro-apoptotic effect and ameliorate growing of cancer cells. Helicobacter pylori (H. pylori) is a main etiologic agent for gastric inflammation, and raises cell turnover in gastric epithelium. Longstanding infection with this organism is related with the development of non-cardiac gastric cancer. The aim of this study was to investigate the effect of H. pylori on the expression of PPARgamma protein and mRNA in chronic gastritis. METHODS: Gastric biopsy samples were taken from H. pylori infected (n=18) and non-infected (n=21) patients during endoscopic examination. PPARgamma expressions were assessed by real time polymerase chain reaction and immunohistochemistry. RESULTS: PPARgamma was localized to the nuclei of the foveolar epithelial cells in both infected and non-infected mucosa. PPARgamma protein expression was higher in H. pylori infected patients than in non-infected patients (3.8+/-0.4 vs. 2.6+/-1.0, H. pylori infected and non-infected, respectively; p<0.05). However, PPARgamma mRNA levels were not significantly different between the two groups (24+/-18 vs. 29+/-25, H. pylori infected and noninfected, respectively). CONCLUSIONS: PPARgamma expression is increased in the gastric mucosa of H. pylori infected chronic gastritis, which suggests a certain role of PPARgamma in the mucosal inflammatory reaction to H. pylori infection.
