Uterine glands are essential for the establishment of pregnancy and have critical roles in endometrial receptivity to blastocyst implantation, stromal cell decidualization, and placentation. Uterine gland dysfunction is considered a major contributing factor to pregnancy loss, however our understanding of how glands impact embryo survival and stromal cell decidualization is incomplete. Forkhead box A2 (FOXA2) is expressed only in the glandular epithelium and regulates its development and function. Mice with a conditional deletion of FOXA2 in the uterus are infertile due to defective embryo implantation arising from a lack of leukemia inhibitory factor (LIF), a critical factor of uterine gland origin. Here, a glandless FOXA2-deficient mouse model, coupled with LIF repletion to rescue the implantation defect, was used to investigate the roles of uterine glands in embryo survival and decidualization. Studies found that embryo survival and decidualization were compromised in glandless FOXA2-deficient mice on gestational day 6.5, resulting in abrupt pregnancy loss by day 7.5. These findings strongly support the hypothesis that uterine glands secrete factors other than LIF that impact embryo survival and stromal cell decidualization for pregnancy success.

中文翻译：

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子宫腺体影响小鼠胚胎存活和基质细胞蜕膜化

子宫腺体对于妊娠的建立至关重要，并且在子宫内膜对胚泡着床、基质细胞蜕膜化和胎盘的接受性方面具有关键作用。子宫腺体功能障碍被认为是导致流产的主要因素，但我们对腺体如何影响胚胎存活和基质细胞蜕膜化的理解尚不完整。Forkhead box A2 (FOXA2) 仅在腺上皮中表达并调节其发育和功能。由于缺乏白血病抑制因子 (LIF)（子宫腺起源的关键因素）导致胚胎植入缺陷，因此在子宫中条件性缺失 FOXA2 的小鼠无法生育。在这里，一个无腺体 FOXA2 缺陷小鼠模型，加上 LIF 补充以挽救植入缺陷，用于研究子宫腺体在胚胎存活和蜕膜化中的作用。研究发现，无腺 FOXA2 缺陷小鼠在妊娠第 6.5 天的胚胎存活和蜕膜化受到损害，导致在第 7.5 天突然流产。这些发现有力地支持了这样一种假设，即子宫腺体分泌的因子不是 LIF，这些因子会影响胚胎存活和基质细胞蜕膜化以成功怀孕。