15-Deoxy-Delta(12,14)-prostaglandin J(2) and troglitazone regulation of the release of phospholipid metabolites, inflammatory cytokines and proteases from human gestational tissues

Placenta. 2006 Nov-Dec;27(11-12):1060-72. doi: 10.1016/j.placenta.2005.11.009. Epub 2006 Jan 23.

Abstract

Phospholipid-derived mediators, inflammatory cytokines and extracellular matrix remodelling enzymes are all involved in the initiation of human labour and delivery. We have previously demonstrated that natural and synthetic PPAR-gamma ligands regulate LPS-stimulated pro-inflammatory cytokine release from human gestational tissues, however, the effect of these ligands on the basal and/or LPS-induced expression of prostaglandins and proteases is not known. Therefore, the aim of this study was to determine the effects of 15d-PGJ(2) and troglitazone on the expression of basal and LPS-stimulated inflammatory mediators in human gestational tissues. Human placenta, amnion and choriodecidua (n=5) were incubated in the presence or absence of 15 microM 15d-PGJ(2) and 30 microM troglitazone under basal and LPS-stimulated (10 microg/ml) conditions. Treatment of placenta, amnion and choriodecidua with both 15d-PGJ(2) and troglitazone decreased basal and LPS-stimulated IL-1beta, IL-6, IL-10 and TNF-alpha release. Basal type II PLA(2) release from placental tissues was also significantly decreased by 15d-PGJ(2) and troglitazone. There was no effects of 15d-PGJ(2) and troglitazone on cPLA(2) protein expression. Both 15d-PGJ(2) and troglitazone significantly decreased basal and LPS-stimulated PGE(2) and PGF(2alpha) release from placenta and amnion. However, in choriodecidua, although 15d-PGJ(2) decreased basal and/or LPS-stimulated PGE(2) and PGF(2alpha) release, there was an increase in PGE(2) and PGF(2alpha) release in the presence of troglitazone. 15d-PGJ(2) and troglitazone inhibited MMP-9 release from human amnion. NF-kappaB DNA binding activity and NF-kappaB p65 protein expression was inhibited by treatment with 15d-PGJ(2) in human amnion. There was no effect of 15d-PGJ(2) or troglitazone on PPAR-gamma protein, and GW9662 failed to alleviate 15d-PGJ(2) and troglitazone inhibition of IL-6 and TNF-alpha release in placenta, amnion and choriodecidua. The data demonstrated in this study suggest that the 15d-PGJ(2) and troglitazone exhibit anti-inflammatory properties in human gestational tissues via PPAR-gamma independent actions.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Anilides / pharmacology
  • Chromans / pharmacology*
  • Cytokines / metabolism*
  • Dinoprost / metabolism
  • Dinoprostone / metabolism
  • Extraembryonic Membranes / drug effects
  • Extraembryonic Membranes / metabolism
  • Female
  • Humans
  • Inflammation / prevention & control
  • Interleukins / metabolism
  • Lipopolysaccharides / pharmacology
  • Matrix Metalloproteinases / metabolism
  • Mitogen-Activated Protein Kinases / metabolism
  • NF-kappa B / metabolism
  • PPAR gamma / antagonists & inhibitors
  • PPAR gamma / physiology
  • Phospholipases A / metabolism
  • Phospholipids / metabolism*
  • Placenta / drug effects
  • Placenta / metabolism*
  • Pregnancy
  • Prostaglandin D2 / analogs & derivatives*
  • Prostaglandin D2 / pharmacology
  • Thiazolidinediones / pharmacology*
  • Troglitazone

Substances

  • 15-deoxy-delta(12,14)-prostaglandin J2
  • 2-chloro-5-nitrobenzanilide
  • Anilides
  • Chromans
  • Cytokines
  • Interleukins
  • Lipopolysaccharides
  • NF-kappa B
  • PPAR gamma
  • Phospholipids
  • Thiazolidinediones
  • Dinoprost
  • Mitogen-Activated Protein Kinases
  • Phospholipases A
  • Matrix Metalloproteinases
  • Troglitazone
  • Dinoprostone
  • Prostaglandin D2