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

被引:37
作者
Nakamuta, M
Enjoji, M
Uchimura, K
Ohta, S
Sugimoto, R
Kotoh, K
Kato, M
Irie, T
Muta, T
Nawata, H
机构
[1] Kyushu Univ, Grad Sch Med Sci, Dept Med & Bioregulatory Sci, Higashi Ku, Fukuoka 8128582, Japan
[2] Kyushu Univ, Grad Sch Med Sci, Dept Mol & Cellular Biochem, Fukuoka, Japan
关键词
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;
D O I
10.1006/cbir.2001.0838
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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.
引用
收藏
页码:235 / 241
页数:7
相关论文
共 30 条
[1]   Bisphenol A diglycidyl ether (BADGE) is a PPARγ agonist in an ECV304 cell line [J].
Bishop-Bailey, D ;
Hla, T ;
Warner, TD .
BRITISH JOURNAL OF PHARMACOLOGY, 2000, 131 (04) :651-654
[2]   Differential activation of peroxisome proliferator-activated receptor-γ by troglitazone and rosiglitazone [J].
Camp, HS ;
Li, O ;
Wise, SC ;
Hong, YH ;
Frankowski, CL ;
Shen, XQ ;
Vanbogelen, R ;
Leff, T .
DIABETES, 2000, 49 (04) :539-547
[3]   PPAR-γ dependent and independent effects on macrophage-gene expression in lipid metabolism and inflammation [J].
Chawla, A ;
Barak, Y ;
Nagy, L ;
Liao, D ;
Tontonoz, P ;
Evans, RM .
NATURE MEDICINE, 2001, 7 (01) :48-52
[4]   15-DEOXY-DELTA(12,14)-PROSTAGLANDIN J(2) IS A LIGAND FOR THE ADIPOCYTE DETERMINATION FACTOR PPAR-GAMMA [J].
FORMAN, BM ;
TONTONOZ, P ;
CHEN, J ;
BRUN, RP ;
SPIEGELMAN, BM ;
EVANS, RM .
CELL, 1995, 83 (05) :803-812
[5]  
Goldman PS, 1997, RECENT PROG HORM RES, V52, P103
[6]   TAK1 mediates an activation signal from toll-like receptor(s) to nuclear factor-κB in lipopolysaccharide-stimulated macrophages [J].
Irie, T ;
Muta, T ;
Takeshige, K .
FEBS LETTERS, 2000, 467 (2-3) :160-164
[7]   PPAR-γ agonists inhibit production of monocyte inflammatory cytokines [J].
Jiang, CY ;
Ting, AT ;
Seed, B .
NATURE, 1998, 391 (6662) :82-86
[8]   A PROSTAGLANDIN J(2) METABOLITE BINDS PEROXISOME PROLIFERATOR-ACTIVATED RECEPTOR-GAMMA AND PROMOTES ADIPOCYTE DIFFERENTIATION [J].
KLIEWER, SA ;
LENHARD, JM ;
WILLSON, TM ;
PATEL, I ;
MORRIS, DC ;
LEHMANN, JM .
CELL, 1995, 83 (05) :813-819
[9]   CONVERGENCE OF 9-CIS RETINOIC ACID AND PEROXISOME PROLIFERATOR SIGNALING PATHWAYS THROUGH HETERODIMER FORMATION OF THEIR RECEPTORS [J].
KLIEWER, SA ;
UMESONO, K ;
NOONAN, DJ ;
HEYMAN, RA ;
EVANS, RM .
NATURE, 1992, 358 (6389) :771-774
[10]   RETRACTED: Ligand type-specific interactions of peroxisome proliferator-activated receptor γ with transcriptional coactivators (Retracted Article) [J].
Kodera, Y ;
Takeyama, K ;
Murayama, A ;
Suzawa, M ;
Masuhiro, Y ;
Kato, S .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (43) :33201-33204