首页> 美国卫生研究院文献>Scientific Reports >MiR-125b regulates endometrial receptivity by targeting MMP26 in women undergoing IVF-ET with elevated progesterone on HCG priming day
【2h】

MiR-125b regulates endometrial receptivity by targeting MMP26 in women undergoing IVF-ET with elevated progesterone on HCG priming day

机译:MiR-125b通过在HCG启动日接受孕酮升高的IVF-ET的妇女靶向MMP26来调节子宫内膜的接受性

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务,本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文,但由于OA文献来源多样且变更频繁,仍可能出现获取不到、文献不完整或与标题不符等情况,如果获取不到我们将提供退款服务。请知悉。
获取外文期刊封面目录资料

摘要

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 effect in 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-125b in vivo and in 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.
机译:在人绒毛膜促性腺激素启动中接受孕酮升高而进行IVF-ET的妇女中,辅助生殖技术的效果较差。但是,由于该过程的机制未知,因此尚未找到有效的方法来克服这一困难。在这里,我们调查了miR-125b及其靶基因MMP26在这些妇女的子宫内膜容受性(ER)中的作用。 miR-125b的表达在植入窗口期间孕酮水平升高的女性的EEC中明显上调,并且在体外显示出孕激素依赖性作用。同样,miR-125b的表达在植入前期明显升高,而在小鼠EECs的植入期和植入后期均下调。另外,miR-125b在植入部位的减少比在植入间部位的减少更大。荧光素酶报告测定法证明MMP26是miR-125b的靶基因。 MMP26的表达谱在体内外均与miR-125b呈负相关。 miR-125b在人EEC中的过表达抑制细胞迁移和侵袭。 miR-125b的功能获得诱导植入部位数量的显着减少。总之,这些数据为miR-125b如何通过调节MMP26功能引发ER下降提供了新的思路。

著录项

相似文献

  • 外文文献
  • 中文文献
代理获取

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号