4.4 Article

Bisphenol a diglycidyl ether (BADGE) suppresses tumor necrosis factor-alpha production as a PPAR gamma agonist in the murine macrophage-like cell line, raw 264.7

Journal

CELL BIOLOGY INTERNATIONAL
Volume 26, Issue 3, Pages 235-241

Publisher

ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
DOI: 10.1006/cbir.2001.0838

Keywords

peroxisome proliferator-activated receptor gamma (PPAR gamma); bisphenol A diglycidyl ether (BADGE); lipopolysaccharide (LPS); tumor necrosis factor-alpha (TNF-alpha); nuclear factor-kappaB (NF-kappa B); coactivator

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Bisphenol A diglycidyl ether (BADGE) is a newly described peroxisome proliferator-activated receptor gamma (PPARgamma) antagonist in adipogenic cells. In contrast, in the macrophage-like cell line RAW 264.7, BADGE, like the PPARgamma agonist pioglitazone hydrochloride, not only increased promoter activity of the PPARgamma-luciferase reporter gene, but also suppressed lipopolysaccharide (LPS)-induced tumor necrosis factor-alpha (TNF-alpha) production. These results suggest that BADGE is a PPARgamma 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-kappaB)-luciferase reporter gene, suggesting that PPARgamma may interfere with NF-kappaB transcriptional activity via coactivator competition. (C) 2002 Elsevier Science Ltd. All rights reserved.

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