Activation of nuclear receptors by prostaglandins

Thromb Res. 2003 Jun 15;110(5-6):311-5. doi: 10.1016/s0049-3848(03)00418-3.

Abstract

Deletion of membrane receptors for prostaglandins has revealed their importance in diverse biological systems. Some evidence has accrued to support the contention that they may also ligate nuclear receptors, particularly peroxisomal proliferator activator receptors (PPARs). This is most pronounced in the case of 15-deoxy PGJ2, a cyclopentanone derivative of PGJ2 as a ligand for PPARgamma. However, while this compound can ligate the PPAR, the quantities formed in vivo suggest that this is an unlikely endogenous ligand. Furthermore, biosynthesis is unaltered in murine atherosclerosis and other inflammatory and metabolic disorders where activation of this PPAR has been implicated. The suggestion that prostaglandins serve as endogenous ligands for nuclear receptors is presently configured on the use of synthetic compounds and immunoreactive quantitation of dubious validity. The application of quantitatively precise and sensitive physicochemical methodology will enhance experiments designed to address this hypothesis.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Prostaglandin D2 / analogs & derivatives
  • Prostaglandin D2 / metabolism
  • Prostaglandin-Endoperoxide Synthases / metabolism*
  • Prostaglandins / metabolism*
  • Receptors, Cytoplasmic and Nuclear / metabolism*
  • Transcription Factors / metabolism

Substances

  • 15-deoxy-delta(12,14)-prostaglandin J2
  • Prostaglandins
  • Receptors, Cytoplasmic and Nuclear
  • Transcription Factors
  • Prostaglandin-Endoperoxide Synthases
  • Prostaglandin D2