Department of Cell and Developmental Biology, University of Illinois-Urbana-Champaign, Urbana, Illinois 61801, USA.
Semin Reprod Med. 2010 Jan;28(1):17-26. doi: 10.1055/s-0029-1242989. Epub 2010 Jan 26.
In murine and human pregnancies, embryos implant by attaching to the luminal epithelium and invading into the stroma of the endometrium. Under the influence of the steroid hormones estrogen and progesterone, the stromal cells surrounding the implanting embryo undergo a remarkable transformation event. This process, known as decidualization, is an essential prerequisite for implantation. It comprises morphogenetic, biochemical, and vascular changes driven by the estrogen and progesterone receptors. The development of mutant mouse models lacking these receptors has firmly established the necessity of steroid signaling for decidualization. Genomic profiling of mouse and human endometrium has uncovered a complex yet highly conserved network of steroid-regulated genes that supports decidualization. To advance our understanding of the mechanisms regulating implantation and better address the clinical challenges of infertility and endometrial diseases such as endometriosis, it is important to integrate the information gained from the mouse and human models.
在鼠类和人类妊娠中,胚胎通过附着在腔上皮并侵入子宫内膜的基质中来着床。在甾体激素雌激素和孕激素的影响下,着床胚胎周围的基质细胞经历显著的转化事件。这个过程称为蜕膜化,是着床的必要前提。它包括形态发生、生化和血管变化,由雌激素和孕激素受体驱动。缺乏这些受体的突变体小鼠模型的发展已经明确了甾体信号对蜕膜化的必要性。对小鼠和人子宫内膜的基因组图谱分析揭示了一个复杂但高度保守的甾体调节基因网络,支持蜕膜化。为了深入了解调控着床的机制,并更好地应对不孕和子宫内膜疾病(如子宫内膜异位症)等临床挑战,将从小鼠和人类模型中获得的信息整合起来非常重要。