Activation of nuclear receptors by prostaglandins

Tomomi Ide, Karine Egan, L. Chastine Bell-Parikh, Garret A. FitzGerald

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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 PGJ 2 as a ligand for PPARγ. 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.

Original languageEnglish
Pages (from-to)311-315
Number of pages5
JournalThrombosis Research
Volume110
Issue number5-6
DOIs
Publication statusPublished - Jun 15 2003
Externally publishedYes

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All Science Journal Classification (ASJC) codes

  • Hematology

Cite this

Ide, T., Egan, K., Bell-Parikh, L. C., & FitzGerald, G. A. (2003). Activation of nuclear receptors by prostaglandins. Thrombosis Research, 110(5-6), 311-315. https://doi.org/10.1016/S0049-3848(03)00418-3