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Effect of PPARgamma ligands on the viability of gastric epithelial cells

K Kojima1, T Shimada, Y Mitobe

  • 1Department of Gastroenterology, Dokkyo University School of Medicine, Tochigi, Japan.

Alimentary Pharmacology & Therapeutics
|April 23, 2002
PubMed
Abstract

Insights

Peroxisome proliferator-activated receptor gamma (PPARγ) activation reduces gastric epithelial cell viability and induces apoptosis. This suggests PPARγ is crucial for regulating gastric cell growth and death.

Area of Science:

  • Molecular biology
  • Cell biology
  • Gastroenterology

Background:

  • Peroxisome proliferator-activated receptors (PPAR) are nuclear receptors with known roles in cell growth.
  • PPARγ's role in gastric epithelial cells was previously unestablished, unlike its known function in colonic cells.

Purpose of the Study:

  • To investigate PPARγ expression in gastric epithelial cells.
  • To determine the impact of PPARγ ligands on gastric epithelial cell viability and apoptosis.

Main Methods:

  • Utilized MKN45 and primary rat gastric epithelial cells.
  • Examined PPARγ expression via RT-PCR and Western blot.
  • Assessed cell viability using WST-1 assay and apoptosis with TUNEL assay.
  • Employed troglitazone and 15d-PGJ2 as PPARγ ligands.

Main Results:

  • MKN45 cells expressed all PPAR subtypes; PPARγ ligands significantly decreased cell viability and induced apoptosis.
  • Ligands for PPARα and PPARδ showed no significant effect on cell viability.
  • Primary gastric cells also expressed PPARγ, and its activation reduced cell viability.

Conclusions:

  • PPARγ plays a significant role in regulating both cell growth and apoptosis in gastric epithelial cells.
  • Findings highlight PPARγ as a potential therapeutic target in gastric conditions.

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