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タイトル別表記
ヒト正常子宮内膜、卵巣子宮内膜症およびモデルマウスの内膜症病変におけるSMADの発現に関する検討
SMADs in endometriosis
著者
門田, 友里 徳島大学大学院医学研究科(医学専攻)
Kasai, Kana Tokushima University
Kawakita, Takako Tokushima University
Murayama, Misaki Tokushima University
新家, 朱理 Tokushima University
Sasada, Hikari Tokushima University
Katayama, Sachiko Tokushima University
Nii, Mari Tokushima University
Yamamoto, Shota Tokushima University
野口, 拓樹 Tokushima University
Tamura, Kou Tokushima University
Aoki, Hidenori Tokushima University
Taniguchi, Miyu Tokushima University
Nakagawa, Tomotaka Tokushima University
キーワード
Endometriosis
Suppressor of mothers against decapentaplegic (SMAD)
Suppressor of mothers against decapentaplegic 7 (SMAD7)
Activin A
資料タイプ
学位論文
抄録
Activin A promotes the development of endometriotic lesions in a murine model of endometriosis, and the immunohistochemical localization of phosphorylated suppressor of mothers against decapentaplegic homolog 2/3 (pSMAD2/3) complex in endometriotic lesions has been reported. Activin may therefore be involved in the development and proliferation of endometriotic cells via the SMAD signaling pathway. However, few detailed reports exist on SMAD7 expression in endometriosis. The purpose of this study was to investigate the expression of pSMAD2/3 or pSMAD3 and SMAD7 in the orthotopic human endometrium, ovarian endometriosis, and endometriotic lesions in a murine model and the effect of activin A on pSMAD2/3 and SMAD7 expression. We established an endometriosis murine model via the intraperitoneal administration of endometrial tissue and blood from donor mice. Activin A was intraperitoneally administered to the activin group. We immunohistochemically evaluated orthotopic endometria, ovarian endometriotic tissues, and endometriotic lesions in the murine model followed by western blotting. We found that pSMAD3 and SMAD7 were expressed in ovarian endometriosis and orthotopic endometria from patients with and without endometriosis. In the murine model, endometriotic lesions expressed pSMAD2/3 and SMAD7 in the activin and control groups, and higher SMAD7 expression was found in the activin group. To the best of our knowledge, this study is the first to show that SMAD7 expression is upregulated in endometriosis. In conclusion, these results suggest that activin A activates the SMAD signaling pathway and promotes the development of endometriotic lesions, thus identifying SMAD7 as a potential therapeutic target for endometriosis.
掲載誌名
Endocrine Journal
ISSN
09188959
13484540
出版者
The Japan Endocrine Society
71
4
開始ページ
395
終了ページ
401
発行日
2024
備考
内容要旨・審査要旨・論文本文の公開
本論文は,著者Yuri Kadotaの学位論文として提出され,学位審査・授与の対象となっている。
権利情報
This article is licensed under a Creative Commons [Attribution-NonCommercial-NoDerivatives 4.0 International] license. https://creativecommons.org/licenses/by-nc-nd/4.0/deed.en
出版社版DOI
出版社版URL
フルテキストファイル
言語
eng
著者版フラグ
博士論文全文を含む
文科省報告番号
甲第3797号
学位記番号
甲医第1605号
学位授与年月日
2024-03-22
学位名
博士(医学)
学位授与機関
徳島大学
部局
医学系
病院