title: [Expression of peroxisome proliferator-activated receptor (PPAR) gamma in Helicobacter pylori-infected gastric epithelium].
abstract: OBJECTIVE
  Peroxisome proliferator-activated receptor gamma (PPAR gamma), a nuclear transcription factor, plays a critical role in the regulation of gene expression associated with inflammation and cancer. PPAR gamma is expressed in human gastric cancer as well as in colon cancer. Activation of PPAR gamma 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 PPAR gamma 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. PPAR gamma expressions were assessed by real time polymerase chain reaction and immunohistochemistry.
  
  
  RESULTS
  PPAR gamma was localized to the nuclei of the foveolar epithelial cells in both infected and non-infected mucosa. PPAR gamma 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, PPAR gamma mRNA levels were not significantly different between the two groups (24+/-18 vs. 29+/-25, H. pylori infected and noninfected, respectively).
  
  
  CONCLUSIONS
  PPAR gamma expression is increased in the gastric mucosa of H. pylori infected chronic gastritis, which suggests a certain role of PPAR gamma in the mucosal inflammatory reaction to H. pylori infection.
authors.affiliation: Departments of Internal Medicine, The Catholic University of Korea College of Medicine, Seoul, Korea.
authors.forename: Seong Hyun
authors.initials: SH
authors.lastname: Son
authors.forename: Hyung Keun
authors.initials: HK
authors.lastname: Kim
authors.forename: Jeong Seon
authors.initials: JS
authors.lastname: Ji
authors.forename: Young Seok
authors.initials: YS
authors.lastname: Cho
authors.forename: Sung Soo
authors.initials: SS
authors.lastname: Kim
authors.forename: Hiun Suk
authors.initials: HS
authors.lastname: Chae
authors.forename: Myung Gyu
authors.initials: MG
authors.lastname: Choi
authors.forename: Sok Won
authors.initials: SW
authors.lastname: Han
authors.forename: Kyu Yong
authors.initials: KY
authors.lastname: Choi
authors.forename: In Sik
authors.initials: IS
authors.lastname: Chung
authors.forename: Ok Ran
authors.initials: OR
authors.lastname: Shin
mesh_terms: D000328:Adult; D003110:Colonic Neoplasms / Q000378:metabolism / Q000382:microbiology / Q000473:pathology; D003199:Computer Systems; D005260:Female; D005753:Gastric Mucosa / Q000378:metabolism* / Q000382:microbiology / Q000473:pathology; D005756:Gastritis / Q000378:metabolism* / Q000382:microbiology / Q000473:pathology; D016481:Helicobacter Infections / Q000378:metabolism* / Q000382:microbiology; D016480:Helicobacter pylori; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D047495:PPAR gamma / Q000378:metabolism*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013274:Stomach Neoplasms / Q000378:metabolism / Q000382:microbiology / Q000473:pathology
chemical_list: D047495:PPAR gamma