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15-deoxy-delta12,14-prostaglandin J2-induced apoptosis in amnion-like WISH cells

J Keelan1, R Helliwell, B Nijmeijer

  • 1Liggins Institute and Divisions of Pharmacology, University of Auckland Faculty of Medical and Health Sciences, New Zealand. j.keelan@auckland.ac.nz

Prostaglandins & Other Lipid Mediators
|January 12, 2002
PubMed

Insights

Certain PPAR-gamma ligands, like 15d-PGJ2, induce apoptosis in fetal membrane cells, potentially impacting preterm birth and neonatal sepsis risk. Further research is needed to understand the exact mechanism.

Area of Science:

  • Cell Biology
  • Obstetrics
  • Biochemistry

Background:

  • Premature rupture of fetal membranes is linked to neonatal sepsis and preterm birth.
  • Apoptosis at the rupture site is a proposed contributing factor.

Purpose of the Study:

  • To investigate the apoptotic effects of peroxisome proliferator-activated receptor (PPAR)-gamma ligands on amnion cells.
  • To assess the potency and kinetics of different PPAR-gamma ligands in inducing apoptosis.

Main Methods:

  • WISH cell line used to model amnion cells.
  • Treatment with PPAR-gamma ligands: 15-deoxy-delta12,14PGJ2 (15d-PGJ2), delta12PGJ2, ciglitizone, and rosiglitazone.
  • Morphological and biochemical assessment of apoptosis, including caspase activation and cell viability assays.

Main Results:

  • 15d-PGJ2 induced significant apoptosis (approx. 60% cell death) with an EC50 of ~7 microM.
  • Delta12-PGJ2 also induced apoptosis, but was less potent and slower acting.
  • Ciglitizone showed some apoptotic effect, while rosiglitazone had no impact on cell viability.

Conclusions:

  • 15d-PGJ2 is a potent inducer of apoptosis in amnion-like cells.
  • The mechanism of apoptosis induction by 15d-PGJ2 and delta12PGJ2 may not solely depend on PPAR-gamma activation.
  • Further studies are required to fully elucidate the apoptotic pathways involved.

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