Molecular Signaling in Decidualization

子宫间质细胞蜕膜化是胚胎着床成功的关键，也是妊娠成功的关键。该过程的特征在于基质细胞增殖并分化为具有多倍性的蜕膜细胞。尽管包括细胞周期蛋白D3（细胞周期调节因子）、HB-EGF（肝素结合EGF样生长因子）和Hoxa-10（同源异型蛋白）在内的各种信号分子参与了蜕膜化，但除了Hoxa-10在此过程中的重要作用外，这些因子调节此过程的确切机制以及它们是否对蜕膜化至关重要尚不清楚。我们假设，蜕膜化的成功是依赖于积极和消极的监管机构之间的平衡，指导增殖和分化至关重要的这一过程，这种平衡的倾斜将导致有缺陷的蜕膜化。我们建议，Hoxa-10和HB-EGF信号收敛到一个共同的下游细胞周期调节电路，包括一个积极的细胞周期调节细胞周期蛋白D3和细胞周期调节细胞周期蛋白G1，以适当地平衡增殖和分化，实现完整的补充蜕膜化。

Uterine stromal cell decidualization is integral to successful embryo implantation which is gateway to pregnancy establishment. This process is characterized by stromal cell proliferation and differentiation into decidual cells with polyploidy. Although various signaling molecules including cyclin D3 (a cell cycle regulator), HB-EGF (a heparinbinding EGF-like growth factor) and Hoxa-10 (a homeotic protein) are implicated in decidualization, the precise mechanisms by which these factors regulate this process and whether they are critical to decidualization are not known, except the essential role of Hoxa-10 in this process. We hypothesize that the success of decidualization is dependent on a balance between positive and negative regulators, directing proliferation and differentiation essential to this process; a tipping of this balance will lead to defective decidualization. We propose that Hoxa-10 and HB-EGF signaling converge to a common downstream cell cycle regulatory circuitry consisting of a positive cell cycle regulator cyclin D3 and negative cell cycle regulator cyclin G1 to appropriately balance proliferation and differentiation for achieving full complement of decidualization.