Bisphenol A diglycidyl ether (BADGE) is a PPARγ agonist in an ECV304 cell line

Authors

  • David Bishop-Bailey,

    Corresponding author
    1. Department 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
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  • Timothy Hla,

    1. Center for Vascular Biology, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, Connecticut, CT 06030-3505, U.S.A.
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  • Timothy D Warner

    1. Department 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
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Department 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. E-mail: 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, PPARγ, 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 PPARγ agonists, 15-deoxy-Δ12,14 PGJ2, and ciglitizone, by inducing luciferase expression. Furthermore, using ECV-ACO.Luc, we demonstrate that a newly described PPARγ antagonist, bisphenol A diglycidyl ether (BADGE) has agonist activities. Similar to 15-deoxy-Δ12,14 PGJ2, BADGE induces PPARγ activation, nuclear localization of the receptor, and induces cell death.

British Journal of Pharmacology (2000) 131, 651–654; doi:10.1038/sj.bjp.0703628

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