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

Makoto Nakamuta, Munechika Enjoji, Koutaro Uchimura, Satoshi Ohta, Rie Sugimoto, Kazuhiro Kotoh, Masaki Kato, Takashi Irie, Tatsushi Muta, Hajime Nawata

Research output: Contribution to journalArticlepeer-review

27 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)235-241
Number of pages7
JournalCell Biology International
Volume26
Issue number3
DOIs
Publication statusPublished - 2002 Jan 1

Keywords

  • Bisphenol A diglycidyl ether (BADGE)
  • Coactivator
  • Lipopolysaccharide (LPS)
  • Nuclear factor-kappaB (NF-κB)
  • Peroxisome proliferator-activated receptor gamma (PPARγ)
  • Tumor necrosis factor-α (TNF-α)

ASJC Scopus subject areas

  • Cell Biology

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