Endometriosis is a benign gynaecological disease appearing with pelvic pain, rising dysmenorrhoea and infertility seriously impacting on 10% of reproductive‐age females. This research attempts to demonstrate the function and molecular mechanism of RhoA/ROCK pathway on epithelial‐mesenchymal transition (EMT) and proliferation in endometriosis. The expression of Rho family was abnormally changed in endometriotic lesions; in particular, RhoA and ROCK1/2 were significantly elevated. Overexpression of RhoA in human eutopic endometrial epithelial cells (eutopic EECs) enhanced the cell mobility, epithelial‐mesenchymal transition (EMT) and proliferation, and RhoA knockdown exhibited the opposite function. Oestrogen up‐regulated the RhoA activity and expression of RhoA and ROCK1/2. RhoA overexpression reinforced the effect of oestrogen on promoting EMT and proliferation, and RhoA knockdown impaired the effect of oestrogen. oestrogen receptor α (ERα) was involved with the regulation of oestrogen on EMT and proliferation and up‐regulated RhoA activity and expression of RhoA and ROCK1/2. The function of ERα was modulated by the change in RhoA expression. Furthermore, phosphorylated ERK that was enhanced by oestrogen and ERα promoted the protein expression of RhoA/ROCK pathway. Endometriosis mouse model revealed that oestrogen enhanced the size and weight of endometriotic lesions. The expression of RhoA and phosphorylated ERK in mouse endometriotic lesions was significantly elevated by oestrogen. We conclude that abnormal activated RhoA/ROCK pathway in endometriosis is responsible for the function of oestrogen/ERα/ERK signalling, which promoted EMT and proliferation and resulted in the development of endometriosis.

中文翻译：

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RhoA/ROCK 通路介导雌激素对调节子宫内膜异位症上皮间质转化和增殖的影响。

子宫内膜异位症是一种以盆腔疼痛、痛经加重和不孕症为主要表现的妇科良性疾病，严重影响了10%的育龄女性。本研究试图证明 RhoA/ROCK 通路对子宫内膜异位症上皮间质转化 (EMT) 和增殖的功能和分子机制。Rho家族在子宫内膜异位病变中表达异常；尤其是 RhoA 和 ROCK1/2 显着升高。RhoA 在人在位子宫内膜上皮细胞 (在位 EECs) 中的过表达增强了细胞迁移率、上皮间质转化 (EMT) 和增殖，而 RhoA 敲低则表现出相反的功能。雌激素上调 RhoA 活性和 RhoA 和 ROCK1/2 的表达。RhoA 过表达增强了雌激素对促进 EMT 和增殖的作用，而 RhoA 敲低会削弱雌激素的作用。雌激素受体α (ERα) 参与雌激素对 EMT 和增殖的调节，并上调 RhoA 活性和 RhoA 和 ROCK1/2 的表达。ERα 的功能受 RhoA 表达变化的调节。此外，雌激素和ERα增强的磷酸化ERK促进了RhoA/ROCK途径的蛋白质表达。子宫内膜异位症小鼠模型显示，雌激素增加了子宫内膜异位病变的大小和重量。RhoA 和磷酸化 ERK 在小鼠子宫内膜异位病变中的表达被雌激素显着升高。