Effect of PPARγ ligands on the viability of gastric epithelial cells
Authors: Kojima, K.1; Shimada, T.1; Mitobe, Y.1; Yoshiura, K.1; Hiraishi, H.1; Terano, A.1
Source: Alimentary Pharmacology & Therapeutics, Volume 16, Supplement 2, April 2002 , pp. 67-73(7)
Publisher: Blackwell Publishing
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Abstract:
Backgournd: Peroxisome proliferator-activated receptors (PPAR) are a family of three nuclear receptors (PPARα, PPARδ, and PPARγ). Although recent evidence suggests a role for PPARγ in the regulation of colonic epithelial cell growth, the role for PPARγ in the stomach has not been established. Aim: To examine the expression of PPARγ and the effects of PPARγ ligands on the viability of gastric epithelial cells. Methods: MKN45 cells and primary cultured rat gastric epithelial cells were used. Troglitazone (TGZ) and 15-deoxy-Δ 12, 14-prostaglandin J2 (15d-PGJ2) were used as PPARγ ligands. Expression of PPARγ was examined by RT-PCR and Western blot analysis. Cell viability was measured by WST-1 assay and TUNEL assay was performed to detect apoptosis. Results: MKN45 cells expressed all subtypes of PPAR. PPARγ ligands decreased cell viability and induced cell death in a dose-dependent manner, whereas ligands for PPARα and PPARδ had no significant effect. TUNEL assay showed that this cell death is apoptosis. Primary cultured rat gastric epithelial cells also expressed PPARγ and activation of PPARγ decreased cell viability. Conclusion: These results suggest that PPARγ plays an important role in the regulation of cell growth and cell death in gastric epithelial cells.Document Type: Research article
DOI: 10.1046/j.1365-2036.16.s2.16.x
Affiliations: 1: Department of Gastroenterology, Dokkyo University School of Medicine, Tochigi, Japan
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