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Genetically-encoded Molecular Probes to Study G Protein-coupled Receptors
Published on: September 13, 2013
Bisphenol A diglycidyl ether (BADGE) is a PPARgamma agonist in an ECV304 cell line
D Bishop-Bailey1, T Hla, T D Warner
1Department of Cardiac, Vascular and Inflammation Research, William Harvey Research Institute, St. Bartholomew's and the Royal London School of Medicine and Dentistry, Charterhouse Square, London, EC1M 6BQ, UK. d.bishop-bailey@mds.qmw.ac.uk
Abstract:
Peroxisome proliferator activated receptors (PPAR)s are nuclear transcription factors of the steroid receptor super-family. One member, PPARgamma, a critical transcription factor in adipogenesis, is expressed in ECV304 cells, and when activated participates in the induction of cell death by apoptosis. Here we describe a clone of ECV304 cells, ECV-ACO.Luc, which stably expresses a reporter gene for PPAR activation. ECV-ACO.Luc respond to the PPARgamma agonists, 15-deoxy-Delta(12,14) PGJ(2), and ciglitizone, by inducing luciferase expression. Furthermore, using ECV-ACO.Luc, we demonstrate that a newly described PPARgamma antagonist, bisphenol A diglycidyl ether (BADGE) has agonist activities. Similar to 15-deoxy-Delta(12,14) PGJ(2), BADGE induces PPARgamma activation, nuclear localization of the receptor, and induces cell death.
