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ID 119335
Title Alternative
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
Author
Kadota, Yuri Tokushima University
Kasai, Kana Tokushima University
Kawakita, Takako Tokushima University
Murayama, Misaki Tokushima University
Shinya, Akari Tokushima University
Sasada, Hikari Tokushima University
Katayama, Sachiko Tokushima University
Nii, Mari Tokushima University
Yamamoto, Shota Tokushima University
Noguchi, Hiroki Tokushima University
Tamura, Kou Tokushima University
Aoki, Hidenori Tokushima University
Taniguchi, Miyu Tokushima University
Nakagawa, Tomotaka Tokushima University
Keywords
Endometriosis
Suppressor of mothers against decapentaplegic (SMAD)
Suppressor of mothers against decapentaplegic 7 (SMAD7)
Activin A
Content Type
Thesis or Dissertation
Description
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.
Journal Title
Endocrine Journal
ISSN
09188959
13484540
Publisher
The Japan Endocrine Society
Volume
71
Issue
4
Start Page
395
End Page
401
Published Date
2024
Remark
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。
Rights
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
DOI (Published Version)
URL ( Publisher's Version )
FullText File
language
eng
TextVersion
ETD
MEXT report number
甲第3797号
Diploma Number
甲医第1605号
Granted Date
2024-03-22
Degree Name
Doctor of Medical Science
Grantor
Tokushima University
departments
Medical Sciences
University Hospital