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BISPHENOL A DIGLYCIDYL ETHER (BADGE) SUPPRESSES TUMOR NECROSIS FACTOR‐α PRODUCTION AS A PPARγ AGONIST IN THE MURINE MACROPHAGE‐LIKE CELL LINE, RAW 264.7
Author(s) -
Nakamuta Makoto,
Enjoji Munechika,
Uchimura Koutaro,
Ohta Satoshi,
Sugimoto Rie,
Kotoh Kazuhiro,
Kato Masaki,
Irie Takashi,
Muta Tatsushi,
Nawata Hajime
Publication year - 2002
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1006/cbir.2001.0838
Subject(s) - agonist , peroxisome proliferator activated receptor , transactivation , tumor necrosis factor alpha , coactivator , reporter gene , pioglitazone , cell culture , chemistry , nuclear receptor , endocrinology , microbiology and biotechnology , biology , medicine , receptor , gene expression , transcription factor , biochemistry , gene , genetics , type 2 diabetes , diabetes mellitus
Bisphenol A diglycidyl ether (BADGE) is a newly described peroxisome proliferator‐activated receptor γ (PPARγ) antagonist in adipogenic cells. In contrast, in the macrophage‐like cell line RAW 264.7, BADGE, like the PPARγ agonist pioglitazone hydrochloride, not only increased promoter activity of the PPARγ‐luciferase reporter gene, but also suppressed lipopolysaccharide (LPS)‐induced tumor necrosis factor‐α (TNF‐α) production. These results suggest that BADGE is a PPARγ agonist in RAW 264.7 cells. Furthermore, overexpression of the coactivator p300 restored BADGE‐ or pioglitazone hydrochloride‐suppressed promoter activity of the nuclear factor‐kappa B (NF‐κB)‐luciferase reporter gene, suggesting that PPARγ may interfere with NF‐κB transcriptional activity via coactivator competition.