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小鼠宫腔粘连模型中telocytes的组织学研究及其对体外间充质干细胞的积极作用。

Histological study of telocytes in mice intrauterine adhesion model and their positive effect on mesenchymal stem cells in vitro.

作者信息

Wei Xiaojiao, Li Hui, Chen Tianquan, Yang Xiaojun

机构信息

Department of Obstetrics and Gynecology, The First Affiliated Hospital of Soochow University, Suzhou City, Jiangsu Province, People's Republic of China.

Department of Obstetrics and Gynecology, The Affiliated Hospital of Yangzhou University, Yangzhou City, Jiangsu Province, People's Republic of China.

出版信息

Cell Biol Int. 2024 May;48(5):647-664. doi: 10.1002/cbin.12137. Epub 2024 Feb 14.

DOI:10.1002/cbin.12137
PMID:38353345
Abstract

Intrauterine adhesions (IUA), the main cause of secondary infertility in women, result from irreversible fibrotic repair of the endometrium due to inflammation or human factors, accompanied by disruptions in the repair function of endometrial stem cells. This significantly impacts the physical and mental health of women in their childbearing years. Telocytes (TCs), a distinctive type of interstitial cells found in various tissues and organs, play diverse repair functions due to their unique spatial structure. In this study, we conduct the inaugural exploration of the changes in TCs in IUA disease and their potential impact on the function of stem cells. Our results show that in vivo, through double immunofluorescence staining (CD34+/Vimentin+; CD34+/CD31-), as endometrial fibrosis deepens, the number of TCs gradually decreases, telopodes shorten, and the three-dimensional structure becomes disrupted in the mouse IUA mode. In vitro, TCs can promote the proliferation and cycle of bone mesenchymal stem cells (BMSCs) by promoting the Wnt/β-catenin signaling pathway, which were inhibited using XAV939. TCs can promote the migrated ability of BMSCs and contribute to the repair of stem cells during endometrial injury. In addition, TCs can inhibit the apoptosis of BMSCs through the Bcl-2/Bax pathway. In conclusion, our study demonstrates, for the first time, the resistance role of TCs in IUA disease, shedding light on their potential involvement in endometrial repair through the modulation of stem cell function.

摘要

宫腔粘连(IUA)是女性继发性不孕的主要原因,由炎症或人为因素导致子宫内膜发生不可逆的纤维化修复,并伴有子宫内膜干细胞修复功能的破坏。这对育龄期女性的身心健康有显著影响。端粒细胞(TCs)是在各种组织和器官中发现的一种独特的间质细胞类型,因其独特的空间结构而发挥多种修复功能。在本研究中,我们首次探索了IUA疾病中端粒细胞的变化及其对干细胞功能的潜在影响。我们的结果表明,在体内,通过双重免疫荧光染色(CD34+/波形蛋白+;CD34+/CD31-),在小鼠IUA模型中,随着子宫内膜纤维化加深,端粒细胞数量逐渐减少,端粒缩短,三维结构遭到破坏。在体外,端粒细胞可通过促进Wnt/β-连环蛋白信号通路来促进骨髓间充质干细胞(BMSCs)的增殖和周期,而XAV939可抑制该通路。端粒细胞可促进骨髓间充质干细胞的迁移能力,并有助于子宫内膜损伤时干细胞的修复。此外,端粒细胞可通过Bcl-2/Bax途径抑制骨髓间充质干细胞的凋亡。总之,我们的研究首次证明了端粒细胞在IUA疾病中的抵抗作用,揭示了它们可能通过调节干细胞功能参与子宫内膜修复。

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