Expression of SMADs in orthotopic human endometrium, ovarian endometriosis, and endometriotic lesions in a murine model

Yuri Kadota, Kadota Y, Kato T, Takeshi Kato, Kana Kasai, Kasai K, Takako Kawakita, Kawakita T, Murayama M, Misaki Murayama, Shinya A, Akari Shinya, Sasada H, Hikari Sasada, Sachiko Katayama, Katayama S, Mari Nii, Nii M, Shota Yamamoto, Yamamoto S, Hiroki Noguchi, Noguchi H, Tamura K, Kou Tamura, Aoki H, Hidenori Aoki, Taniguchi M, Miyu Taniguchi, Tomotaka Nakagawa, Nakagawa T, Kaji T, Takashi Kaji, Masato Nishimura, Nishimura M, Riyo Kinouchi, Kinouchi R, Yoshida K, Kanako Yoshida, Takeshi Iwasa, Iwasa T
Endocrine journal · 2024 · vol. 71(4) , pp. 395–401 · doi:10.1507/endocrj.ej23-0486 · PMID:38417880 · W4392208244
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⚙ AI-generated summary by gemini-2.5-flash-lite, 2026-07-21 ⓘ

This study investigated SMAD3 and SMAD7 expression in human endometrium and a murine endometriosis model, finding SMAD7 upregulated in endometriosis and suggesting activin A activates the SMAD pathway to promote lesion development.

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⚙ AI-generated deep summary by qwen3.7-flash, 2026-08-21 · read from full text ⓘ

This study investigated the expression of phosphorylated SMAD2/3 and SMAD7 in orthotopic human endometrium, ovarian endometriosis, and a murine model of endometriosis to understand the role of Activin A. Researchers established an endometriosis murine model by administering endometrial tissue and blood from donor mice, followed by intraperitoneal injection of Activin A. Immunohistochemical evaluation and western blotting revealed that SMAD7 expression was upregulated in endometriotic lesions within the Activin-treated group compared to controls. The findings indicate that Activin A activates the SMAD signaling pathway, promoting lesion development and highlighting SMAD7 as a potential therapeutic target. This paper is centrally about endometriosis — specifically examining molecular mechanisms involving SMAD signaling in ovarian and ectopic lesions.

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Abstract

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.
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Keywords

Endometriosis, Suppressor of mothers against decapentaplegic (SMAD), Suppressor of mothers against decapentaplegic 7 (SMAD7), Activin A 2024 Volume 71 Issue 4 Pages 395-401 Details

Abstract

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. © The Japan Endocrine Society 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 Favorites & Alerts Recently viewed articles Predecessor

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Condition tags

endometriosis

MeSH descriptors

Activins Activins Activins Activins Activins Activins Activins Activins Activins Activins Activins Activins Activins Activins Activins Activins Activins Activins Activins Activins

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