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Effect of PPARγ ligands on the viability of gastric epithelial cells
Article first published online: 20 APR 2002
DOI: 10.1046/j.1365-2036.16.s2.16.x
1365-2036/asset/cover.gif?v=1&s=d621428d7905f55dc6cbe431b6da6a6c8f16399c "Alimentary Pharmacology & Therapeutics")
Additional Information
How to Cite
Kojima, K. , Shimada, T. , Mitobe, Y. , Yoshiura, K. , Hiraishi, H. and Terano, A. (2002), Effect of PPARγ ligands on the viability of gastric epithelial cells. Alimentary Pharmacology & Therapeutics, 16: 67–73. doi: 10.1046/j.1365-2036.16.s2.16.x
Publication History
- Issue published online: 20 APR 2002
- Article first published online: 20 APR 2002
- Abstract
- Article
- References
- Cited By
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-Δ12, 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.