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

Author:

Wei Xiaojiao1ORCID,Li Hui1,Chen Tianquan12,Yang Xiaojun1ORCID

Affiliation:

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

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

Abstract

AbstractIntrauterine 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.

Funder

National Natural Science Foundation of China

Publisher

Wiley

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