The regulation mechanisms involved in matrix metalloproteinase (MMP) expression and the motility of human endometrial and decidual stromal cells (ESCs and DSCs, respectively) during decidualization remain unclear. DSCs show significant increased cell motility and expression of FOS-like 1 (FOSL1) and MMP1, MMP2, and MMP9 compared with ESCs, whereas lack of decidualization inducers leads to a rapid decrease in FOSL1 and MMP1 and MMP9 expression in DSCs in vitro Therefore, we hypothesized that a link exists between decidualization inducers and FOSL1 in up-regulation of motility during decidualization. Based on the response of ESCs/DSCs to different decidualization systems in vitro, we found that progesterone (P4) alone had no significant effect and that 17β-estradiol (E2) significantly increased cell motility and FOSL1 and MMP1 and MMP9 expression at the mRNA and protein levels, whereas 8-bromo-cAMP significantly decreased cell motility and FOSL1 and MMP9 expression in the presence of P4. In addition, we showed that E2 triggered phosphorylation of estrogen receptor 1 (ESR1), which could directly bind to the promoter of FOSL1 in ESCs/DSCs. Additionally, we also revealed silencing of ESR1 expression by siRNA abrogated E2-induced FOSL1 expression at the transcript and protein levels. Moreover, silencing of FOSL1 expression by siRNA was able to block E2-induced MMP1 and MMP9 expression and cell motility in ESCs/DSCs. Taken together, our data suggest that, in addition to its enhancement of secretory function, the change in MMP expression and cell motility is another component of the decidualization of ESCs/DSCs, including estrogen-dependent MMP1 and MMP9 expression mediated by E2-ESR1-FOSL1 signaling.

中文翻译：

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雌激素诱导的FOS样1调节基质金属蛋白酶的表达以及人类子宫内膜和蜕膜基质细胞的运动。

蜕膜化过程中涉及基质金属蛋白酶（MMP）表达以及人类子宫内膜和蜕膜基质细胞（分别为ESCs和DSCs）的运动的调节机制仍不清楚。与ESC相比，DSC显示出明显增强的细胞运动性以及FOS-like 1（FOSL1）和MMP1，MMP2和MMP9的表达，而蜕膜化诱导剂的缺乏导致DSSC的FOSL1和MMP1和MMP9的表达迅速降低。因此，我们假设在蜕膜化过程中，蜕膜化诱导因子和FOSL1之间存在联系。根据ESC / DSC对体外不同蜕膜系统的反应，我们发现单独的孕激素（P4）并没有明显的作用，而17β-雌二醇（E2）在mRNA和蛋白质水平上显着增加了细胞运动性以及FOSL1和MMP1和MMP9的表达，而8-bromo-cAMP显着降低了细胞运动性和FOSL1 P4存在下MMP9和MMP9的表达。此外，我们发现E2触发了雌激素受体1（ESR1）的磷酸化，该磷酸化可以直接与ESC / DSC中FOSL1的启动子结合。此外，我们还揭示了在转录本和蛋白质水平上，siRNA消除了E2诱导的FOSL1表达，从而使ESR1表达沉默。此外，通过siRNA抑制FOSL1表达能够阻止E2诱导的MMP1和MMP9表达以及ESC / DSC中的细胞运动。综上所述，我们的数据表明，除了增强分泌功能外，