Ohtake Fumiaki, Takeyama Ken-ichi, Matsumoto Takahiro, Kitagawa Hirochika, Yamamoto Yasuji, Nohara Keiko, Tohyama Chiharu, Krust Andree, Mimura Junsei, Chambon Pierre, Yanagisawa Junn, Fujii-Kuriyama Yoshiaki, Kato Shigeaki
The Institute of Molecular and Cellular Biosciences, University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo, 113-0032, Japan.
Nature. 2003 May 29;423(6939):545-50. doi: 10.1038/nature01606.
Environmental contaminants affect a wide variety of biological events in many species. Dioxins are typical environmental contaminants that exert adverse oestrogen-related effects. Although their anti-oestrogenic actions are well described, dioxins can also induce endometriosis and oestrogen-dependent tumours, implying possible oestrogenic effects. However, the molecular mechanism underlying oestrogen-related actions of dioxins remains largely unknown. A heterodimer of the dioxin receptor (AhR) and Arnt, which are basic helix-loop-helix/PAS-family transcription factors, mediates most of the toxic effects of dioxins. Here we show that the agonist-activated AhR/Arnt heterodimer directly associates with oestrogen receptors ER-alpha and ER-beta. This association results in the recruitment of unliganded ER and the co-activator p300 to oestrogen-responsive gene promoters, leading to activation of transcription and oestrogenic effects. The function of liganded ER is attenuated. Oestrogenic actions of AhR agonists were detected in wild-type ovariectomized mouse uteri, but were absent in AhR-/- or ER-alpha-/- ovariectomized mice. Our findings suggest a novel mechanism by which ER-mediated oestrogen signalling is modulated by a co-regulatory-like function of activated AhR/Arnt, giving rise to adverse oestrogen-related actions of dioxin-type environmental contaminants.
环境污染物会影响许多物种的多种生物事件。二噁英是典型的环境污染物,会产生与雌激素相关的不良影响。尽管它们的抗雌激素作用已得到充分描述,但二噁英也可诱发子宫内膜异位症和雌激素依赖性肿瘤,这意味着可能存在雌激素效应。然而,二噁英与雌激素相关作用的分子机制在很大程度上仍不清楚。二噁英受体(AhR)和Arnt的异二聚体是碱性螺旋-环-螺旋/PAS家族转录因子,介导了二噁英的大部分毒性作用。在此我们表明,激动剂激活的AhR/Arnt异二聚体直接与雌激素受体ER-α和ER-β结合。这种结合导致未结合配体的ER和共激活因子p300被募集到雌激素反应性基因启动子上,从而导致转录激活和雌激素效应。结合配体的ER的功能减弱。在野生型去卵巢小鼠子宫中检测到AhR激动剂的雌激素作用,但在AhR基因敲除或ER-α基因敲除的去卵巢小鼠中未检测到。我们的研究结果提示了一种新机制,即通过激活的AhR/Arnt的共调节样功能来调节ER介导的雌激素信号传导,从而导致二噁英型环境污染物产生与雌激素相关的不良作用。