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Biochanin A enhances ROR gamma activity through STAT3-mediated recruitment of NCOA1

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Title: Biochanin A enhances ROR gamma activity through STAT3-mediated recruitment of NCOA1
Authors: Takahashi, Miki Browse this author
Muromoto, Ryuta Browse this author →KAKEN DB
Kojima, Hiroyuki Browse this author
Takeuchi, Shinji Browse this author
Kitai, Yuichi Browse this author →KAKEN DB
Kashiwakura, Jun-ichi Browse this author
Matsuda, Tadashi Browse this author →KAKEN DB
Keywords: Isoflavones
IL-17
STAT3
ROR gamma
Issue Date: 5-Aug-2017
Publisher: Elsevier
Journal Title: Biochemical and biophysical research communications
Volume: 489
Issue: 4
Start Page: 503
End Page: 508
Publisher DOI: 10.1016/j.bbrc.2017.05.181
PMID: 28579428
Abstract: Interleukin (IL)-17-producing T cells play important roles in autoimmunity, chronic inflammation and host protection against extracellular bacteria and fungi. The retinoic acid receptor-related orphan receptors (ROR) alpha and beta are key regulators of the IL-17-producing phenotype. We previously showed that the isoflavone biochanin A enhanced ROR-mediated transcriptional activity. Here, we investigated the possible mechanisms underlying this ROR activation. Biochanin A-treated murine thymoma EL4 and primary splenocytes demonstrated enhanced induction of IL-17. Biochanin A also induced tyrosine-phosphorylation of signal transducer and activator of transcription 3 (STAT3) in these cells. Stable knockdown of either ROR gamma or STAT3 in EL4 cells canceled biochanin A-induced upregulation of IL-17 expression. Importantly, biochanin A enhanced complex formation between ROR gamma and STAT3 or nuclear-receptor coactivator 1 (NCOA1). Furthermore, the biochanin A-induced ROR gamma-NCOA1 complex was disrupted by a dominant negative mutant of STAT3 or by the STAT3 specific inhibitor Stattic. These results suggest that biochanin A activates ROR gamma-dependent IL-17 transcription through the enhancement of STAT3 phosphorylation and STAT3-mediated recruitment of NCOA1 to ROR gamma. (C) 2017 Elsevier Inc. All rights reserved.
Rights: ©2017. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/
http://creativecommons.org/licenses/by-nc-nd/4.0/
Type: article (author version)
URI: http://hdl.handle.net/2115/71218
Appears in Collections:薬学研究院 (Faculty of Pharmaceutical Sciences) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 松田 正

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