在胚胎着床期间，胚泡与子宫内膜相互作用并可调节后者，子宫内膜分泌的液体也可为胚胎提供营养。在本研究工作中，研究人员假设成熟的miRNAs可能在其中发挥着调节附着前胚胎转录组的作用。miRNA芯片检测显示27个特异、产妇的miRNAs中有6个在处于着床窗口（一个短暂阶段的子宫内膜接受胚泡）的人子宫内膜中特异表达，并释放到子宫内膜流体中。进一步研究显示，hsa-miR-30d显著上调，并且释放在exosome中。小鼠胚胎可通过滋养外胚层吸收Exosome相关的和游离的hsa-miR-30d，从而导致小鼠胚胎粘附现象相关的基因，Itgb3, Itga7 and Cdh5的表达上调。此外，改发现也通过体外实验证明miR-30d处理的小鼠胚胎具有更强的胚胎粘附能力。由此得出结论，该研究发现产妇子宫内膜miRNAs可调节附着前胚胎的转录组。
原文来源： Vilella, F., et al. (2015). Hsa-miR-30d, secreted by the human endometrium, is taken up by the pre-implantation embryo and might modify its transcriptome. Development 142(18): 3210-3221.
During embryo implantation, the blastocyst interacts with and regulates the endometrium, and endometrial fluid secreted by the endometrial epithelium nurtures the embryo. Here, we propose that maternal microRNAs (miRNAs) might act as transcriptomic modifier of the pre-implantation embryo. Microarray profiling revealed that six of 27 specific, maternal miRNAs were differentially expressed in the human endometrial epithelium during the window of implantation - a brief phase of endometrial receptivity to the blastocyst - and were released into the endometrial fluid. Further investigation revealed that hsa-miR-30d, the expression levels of which were most significantly upregulated, was secreted as an exosome-associated molecule. Exosome-associated and free hsa-miR-30d was internalized by mouse embryos via the trophectoderm, resulting in an indirect overexpression of genes encoding for certain molecules involved in the murine embryonic adhesion phenomenon - Itgb3, Itga7 and Cdh5. Indeed, this finding was supported by evidence in vitro: treating murine embryos with miR-30d resulted in a notable increase in embryo adhesion. Our results suggest a model in which maternal endometrial miRNAs act as transcriptomic modifiers of the pre-implantation embryo.
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