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Effect of PPARγ ligands on the viability of gastric epithelial cells
Author(s) -
Kojima K.,
Shimada T.,
Mitobe Y.,
Yoshiura K.,
Hiraishi H.,
Terano A.
Publication year - 2002
Publication title -
alimentary pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.308
H-Index - 177
eISSN - 1365-2036
pISSN - 0269-2813
DOI - 10.1046/j.1365-2036.16.s2.16.x
Subject(s) - viability assay , troglitazone , peroxisome proliferator activated receptor , apoptosis , receptor , biology , tunel assay , programmed cell death , microbiology and biotechnology , cell growth , medicine , cell culture , endocrinology , biochemistry , genetics
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 J 2 (15d‐PGJ 2 ) 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.