哺乳动物子宫内膜覆盖着腔上内皮（LE），它直接与囊胚相互作用，在着床期间囊胚与接受性子宫之间的相互交流中起着重要作用。然而，在容受期内，囊胚对子宫分化的影响尚不甚了解。通过激光捕获显微切割（LCM）分离的子宫腔上内皮的转录组表征，证明了没有胚胎的伪妊娠小鼠与有胚胎的妊娠小鼠之间的腔上内皮的全局基因表达变化。聚焦表达基因中，一些差异表达的基因在有胚胎的小鼠中上调，包括Areg（amphiregulin），Ihh（Indian hedgehog），Lif（leukemia inhibitory factor），下调的基因有Msx1（msh homeobox 1），Pgr（progesterone receptor），Gata2（GATA binding protein 2），这些基因已被报道与子宫容受性的建立有关。此外，我们还发现囊胚可诱导腔上内皮溶酶体数量及酸化增加，与腔上内皮溶酶体水解酶活性增强相一致。进一步的探索发现，囊胚来源的IGF2参与了上皮细胞STAT3的激活，诱导溶酶体水解酶的表达，而抑制溶酶体功能则会影响子宫容受性标志基因的表达和胚胎着床。最后，根据上皮和分离的溶酶体的蛋白质组数据揭示，CLDN1（claudin 1）和MUC1（mucin 1, transmembrane）两个成功着床过程中已知下调的分子会被上皮细胞溶酶体降解。总之，我们的数据表明囊胚通过激活溶酶体促进了正常的上皮细胞分化，从而促进子宫上皮细胞分化以便于胚胎着床。

The mammalian endometrium is covered by the lumenal epithelium (Le), which directly interacts with the blastocyst and plays an important role in the establishment of reciprocal crosstalk between the embryo and receptive uterus during implantation. However, the effect of the blastocyst on uterine differentiation during the window of receptivity is far from well understood. Through transcriptomic profiling of the uterine Le isolated by laser capture microdissection (LCM), it was demonstrated that global gene expression changes occurred in Le between pseudopregnant mice without embryos and pregnant mice with embryos. Some differentially expressed genes, including upregulated Areg (amphiregulin), Ihh (Indian hedgehog), Lif (leukemia inhibitory factor) and downregulated Msx1 (msh homeobox 1), Pgr (progesterone receptor), and Gata2 (GATA binding protein 2) in pregnant mice, have been reported to regulate the establishment of uterine receptivity. Besides, we found that blastocysts induced an increase in both the number and acidification of lysosome, consistent with enhanced lysosomal hydrolase activity in uterine Le. Further exploration uncovered that blastocyst-derived IGF2 was involved into the activation of epithelial STAT3 to induce lysosomal hydrolase expression, and inhibition of lysosomal function derails both uterine receptive maker gene expressions and embryo implantation. Finally, based on the proteomic data of both epithelia and the separated lysosome, it was revealed that CLDN1 (claudin 1) and MUC1 (mucin 1, transmembrane), two well-known downregulated molecules for successful implantation, are degraded by epithelial lysosome. In brief, our data demonstrated that blastocysts induced normal epithelium differentiation with lysosome activation to promote the uterine epithelial differentiation for embryo implantation.