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

IF 1.3 4区 医学 Q4 ENDOCRINOLOGY & METABOLISM Endocrine journal Pub Date : 2024-02-28 DOI:10.1507/endocrj.ej23-0486
Yuri Kadota, Takeshi Kato, Kana Kasai, Takako Kawakita, Misaki Murayama, Akari Shinya, Hikari Sasada, Sachiko Katayama, Mari Nii, Shota Yamamoto, Hiroki Noguchi, Kou Tamura, Hidenori Aoki, Miyu Taniguchi, Tomotaka Nakagawa, Takashi Kaji, Masato Nishimura, Riyo Kinouchi, Kanako Yoshida, Takeshi Iwasa
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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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SMADs 在正位人类子宫内膜、卵巢子宫内膜异位症和鼠类子宫内膜异位症病变中的表达
在一种子宫内膜异位症小鼠模型中,Activin A 促进了子宫内膜异位症病灶的发展,并且有报道称在子宫内膜异位症病灶中存在磷酸化母细胞抑制因子(phosphorylated suppressor of mothers against decapentaplegic homolog 2/3)复合物(pSMAD2/3)的免疫组织化学定位。因此,Activin 可能通过 SMAD 信号通路参与子宫内膜异位细胞的发育和增殖。然而,有关 SMAD7 在子宫内膜异位症中表达的详细报道却很少。本研究的目的是调查 pSMAD2/3 或 pSMAD3 和 SMAD7 在正位人子宫内膜、卵巢子宫内膜异位症和子宫内膜异位症鼠模型中的表达情况,以及活化素 A 对 pSMAD2/3 和 SMAD7 表达的影响。我们通过腹腔注射供体小鼠的子宫内膜组织和血液建立了子宫内膜异位症小鼠模型。活化素组腹腔注射活化素 A。我们对小鼠模型中的正位子宫内膜、卵巢子宫内膜异位组织和子宫内膜异位病灶进行了免疫组化评估,然后进行了免疫印迹。我们发现,pSMAD3 和 SMAD7 在卵巢子宫内膜异位症患者和非子宫内膜异位症患者的正位子宫内膜中均有表达。在小鼠模型中,活化素组和对照组的子宫内膜异位症病灶均表达 pSMAD2/3 和 SMAD7,其中活化素组的 SMAD7 表达更高。据我们所知,这项研究首次表明 SMAD7 在子宫内膜异位症中表达上调。总之,这些结果表明,激活素 A 可激活 SMAD 信号通路并促进子宫内膜异位症病变的发展,从而确定 SMAD7 是子宫内膜异位症的潜在治疗靶点。
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来源期刊
Endocrine journal
Endocrine journal 医学-内分泌学与代谢
CiteScore
4.30
自引率
5.00%
发文量
224
审稿时长
1.5 months
期刊介绍: Endocrine Journal is an open access, peer-reviewed online journal with a long history. This journal publishes peer-reviewed research articles in multifaceted fields of basic, translational and clinical endocrinology. Endocrine Journal provides a chance to exchange your ideas, concepts and scientific observations in any area of recent endocrinology. Manuscripts may be submitted as Original Articles, Notes, Rapid Communications or Review Articles. We have a rapid reviewing and editorial decision system and pay a special attention to our quick, truly scientific and frequently-citable publication. Please go through the link for author guideline.
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