Placenta · 2022
Exosomal miR-543 derived from umbilical cord mesenchymal stem cells ameliorates endometrial fibrosis in intrauterine adhesion via downregulating N-cadherin.
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Yuan Donglan, Guo Ting, Qian Hua, Jin Chunyan, Ge Hongshan, Zhao Yinling, Zhu Dandan, Lin Mei, Wang Hua, Yu Hong
Аннотация
INTRODUCTION: Human umbilical cord mesenchymal stem cells (UCMSCs) play an important role in repairing the damaged endometrium of intrauterine adhesion (IUA). Meanwhile, exosomes released by UCMSCs can mediate intercellular communication by delivering miRNAs. It has been shown that miR-543 level was reduced in IUA tissues. However, the role of miR-543 in the progression of IUA remains largely unknown. Therefore, we investigated the role of UCMSCs-derived exosomal miR-543 in IUA.
METHODS: In this study, human endometrial epithelial cells (hEECs) were treated with TGF-β1 for mimicking endometrial fibrosis in vitro. In addition, the IUA-like mouse model in vivo was established by a dual damage method of curettage and LPS infection.
RESULTS: The level of miR-543 was markedly reduced in hEECs exposed to TGF-β1 and in endometrium tissues of IUA mice. Additionally, miR-543 could be transferred from UCMSCs to hEECs via exosomes. Meanwhile, exosomal miR-543-derived from UCMSCs significantly reduced the expressions of N-cadherin, α-SMA, fibronectin 1 and elevated the expression of E-cadherin in TGF-β1-treated hEECs. Furthermore, UCMSCs-derived exosomal miR-543 attenuated IUA-induced endometrial fibrosis in vivo, as shown by the decreased N-cadherin, α-SMA and fibronectin 1 protein expressions.
DISCUSSION: Collectively, UCMSCs-derived exosomal miR-543 was able to prevent endometrial fibrosis both in vitro and in vivo via downregulating N-cadherin. These results may provide an insight into the clinical treatment for IUA.
METHODS: In this study, human endometrial epithelial cells (hEECs) were treated with TGF-β1 for mimicking endometrial fibrosis in vitro. In addition, the IUA-like mouse model in vivo was established by a dual damage method of curettage and LPS infection.
RESULTS: The level of miR-543 was markedly reduced in hEECs exposed to TGF-β1 and in endometrium tissues of IUA mice. Additionally, miR-543 could be transferred from UCMSCs to hEECs via exosomes. Meanwhile, exosomal miR-543-derived from UCMSCs significantly reduced the expressions of N-cadherin, α-SMA, fibronectin 1 and elevated the expression of E-cadherin in TGF-β1-treated hEECs. Furthermore, UCMSCs-derived exosomal miR-543 attenuated IUA-induced endometrial fibrosis in vivo, as shown by the decreased N-cadherin, α-SMA and fibronectin 1 protein expressions.
DISCUSSION: Collectively, UCMSCs-derived exosomal miR-543 was able to prevent endometrial fibrosis both in vitro and in vivo via downregulating N-cadherin. These results may provide an insight into the clinical treatment for IUA.