TY - JOUR
T1 - 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
AU - Nakamuta, Makoto
AU - Enjoji, Munechika
AU - Uchimura, Koutaro
AU - Ohta, Satoshi
AU - Sugimoto, Rie
AU - Kotoh, Kazuhiro
AU - Kato, Masaki
AU - Irie, Takashi
AU - Muta, Tatsushi
AU - Nawata, Hajime
N1 - Funding Information:
Kato (University of Tokyo, Tokyo, Japan) for providing the plasmids ACO-PPRE and CMV p300, respectively. We thank Takeda Ltd (Osaka, Japan) for supplying pioglitazone hydrochloride. We also thank K. Tsuru for expert secretarial assistance. This work was supported by a Grant-in-aid (12670498, 12670497) for Scientific Research from the Ministry of Education, Science and Culture, Japan, and by a grant from Mitsui Life Insurance Public Welfare Enterprise, Japan.
PY - 2002
Y1 - 2002
N2 - 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.
AB - 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.
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U2 - 10.1006/cbir.2001.0838
DO - 10.1006/cbir.2001.0838
M3 - Article
C2 - 11991651
AN - SCOPUS:0036393612
SN - 1065-6995
VL - 26
SP - 235
EP - 241
JO - Cell Biology International Reports
JF - Cell Biology International Reports
IS - 3
ER -