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Bisphenol A diglycidyl ether (BADGE) is a PPARγ agonist in an ECV304 cell line
Author(s) -
BishopBailey David,
Hla Timothy,
Warner Timothy D
Publication year - 2000
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1038/sj.bjp.0703628
Subject(s) - agonist , peroxisome proliferator activated receptor , nuclear receptor , transcription factor , receptor , microbiology and biotechnology , adipogenesis , cell culture , ppar agonist , programmed cell death , reporter gene , apoptosis , chemistry , biology , gene expression , biochemistry , gene , genetics , mesenchymal stem cell
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‐Δ 12,14 PGJ 2 , 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‐Δ 12,14 PGJ 2 , 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