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MiR-449a regulates caprine endometrial stromal cell apoptosis and endometrial receptivity

机译:MiR-449a调节小鼠子宫内膜间质细胞凋亡和子宫内膜容受性

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摘要

In this study, an RT-qPCR analysis showed that the expression levels of miR-449a in the pre-receptive endometrium were lower compared to the receptive endometrium, which is consistent with previous sequencing data (previous investigations). To detect the role of miR-449a in endometrial receptivity, we transfected caprine endometrial stromal cells (ESCs) cultured in vitro with miR-449a mimics. The results revealed that miR-449a decreased the mRNA and protein levels of LGR4 by targeting its 3′-untranslated region. The miR-449a mimics significantly reduced the G1 cell population from 52.56% (mimic NC) to 42.19% with a concordant increase in the G2 and S cell populations from 47.44% (mimic NC) to 57.81%, suggesting that miR-449a caused ESC cell cycle arrest. In addition, the number of apoptotic cells was significantly higher in ESCs transfected with miR-449a mimics (P < 0.05) than in ESCs transfected with mimic NC. In vivo, rich pinopodes were observed on the endometrial surface in the miR-449a agomir group compared with the miR-449a antagomir group. The results of hematoxylin-eosin staining showed that endometrial thickness was significantly increased in the miR-449a agomir group compared with the miR-449a antagomir group. These results suggest that miR-449a could enhance endometrial receptivity.
机译:在这项研究中,RT-qPCR分析表明,与受体内膜相比,miR-449a在受体前内膜的表达水平较低,这与以前的测序数据一致(先前的研究)。为了检测miR-449a在子宫内膜接受性中的作用,我们转染了miR-449a模拟物体外培养的山羊子宫内膜基质细胞(ESC)。结果表明,miR-449a通过靶向3R非翻译区降低了LGR4的mRNA和蛋白水平。 miR-449a模拟物显着降低了G1细胞群,从52.56%(模拟NC)降至42.19%,同时G2和S细胞群也从47.44%(模拟NC)增加至57.81%,表明miR-449a引起了ESC细胞周期停滞。另外,用miR-449a模拟物转染的ESC中凋亡细胞的数量显着高于用NC模拟物转染的ESC中(P <0.05)。在体内,与miR-449a antagomir组相比,miR-449a agomir组的子宫内膜表面观察到了丰富的pinodes。苏木精-伊红染色结果显示,与miR-449a antagomir组相比,miR-449a agomir组的子宫内膜厚度显着增加。这些结果表明,miR-449a可以增强子宫内膜的接受能力。

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