MiR-125b regulates endometrial receptivity by targeting MMP26 in women undergoing IVF-ET with elevated progesterone on HCG priming day.
MiR-125b regulates endometrial receptivity by targeting MMP26 in women undergoing IVF-ET with elevated progesterone on HCG priming day.
复制标题
在 HCG 启动日接受 IVF-ET 且黄体酮升高的女性中，MiR-125b 通过靶向 MMP26 来调节子宫内膜容受性
DOI：
10.1038/srep25302
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发表时间：
2016-05-04
影响因子：
4.6
通讯作者：
Qiao J
中科院分区：
文献类型：
--
作者：
Chen C;Zhao Y;Yu Y;Li R;Qiao J
在接受IVF-ET的妇女中，在人绒毛膜促性腺激素预充时孕酮升高，辅助生殖技术的结局较差。但是，由于这一过程的机制尚不清楚，目前还没有找到有效的方法来克服这一困难。在此，我们研究了miR-125 b及其靶基因MMP 26在这些妇女子宫内膜容受性（ER）中的作用。在胚胎着床窗口期，孕酮水平升高的妇女的EECs中miR-125 b的表达显著上调，并在体外表现出孕酮依赖性作用。同样，miR-125 b在小鼠EECs中的表达在着床前显著上调，在着床期和着床后显著下调。此外，miR-125 b在植入部位的下降幅度大于在回植部位的下降幅度。荧光素酶报告试验证明MMP 26是miR-125 b的靶基因。MMP-26的表达与miR-125的表达呈负相关。miR-125 b在人内皮细胞中的过表达抑制了细胞的迁移和侵袭。miR-125 b的功能获得诱导着床位点数量的显著减少。总之，这些数据揭示了miR-125 b如何通过调节MMP 26功能触发ER下降。
On the women undergoing IVF-ET with elevated progesterone on human chorionic gonadotrophin priming, the assisted reproductive technology outcome is poor. But, due to the unknown mechanism of this process, no effective method has been found to overcome this difficulty. Here, we investigated the roles of miR-125b and its target gene, MMP26, in endometrial receptivity (ER) in these women. The expression of miR-125b was significantly up-regulated in EECs in women with elevated progesterone during the window of implantation and it showed a progesterone-dependent effectin vitro. Similarly, the expression of miR-125b was significantly up-regulated in the preimplantation period and was down-regulated in the implantation period and the post-implantation period in mouse EECs. In addition, miR-125b showed a greater decrease at implantation sites than it did at interimplantation sites. The luciferase report assay demonstrated that MMP26 is a target gene of miR-125b. And the expression profile of MMP26 showed an inverse relationship with miR-125bin vivoandin vitro. Overexpression of miR-125b in human EECs inhibited cell migration and invasion. Gain-of-function of miR-125b induced a significant decrease in the number of implantation sites. In conclusion, these data shed new light on how miR-125b triggers ER decline through the regulation of MMP26 function.