UCHL1 is expressed specifically in the brain and gonads of almost all studied model organisms including Drosophila, zebrafish, amphibians, and mammals, suggesting a high degree of evolutionary conservation in its structure and function. Although UCHL1 has been involved in spermatogenesis in mice, its specific expression in mammal placenta remains elusive. Our previous work has revealed that UCHL1 is highly expressed in oocytes, and has been involved in mouse ovarian follicular development. Here, we further examined UCHL1 expression change in endometria during early natural pregnancy, with different stages of the estrous cycle and pseudopregnancy as control. The UCHL1 gene deletion model showed that UCHL1 protein is associated with endometrial development, and its deletion leads to infertility. Notably, we demonstrate evidence showing the distinct expression pattern of UCHL1: weak expression over the uterine endometria, strong expression in decidualized stromal cells at the implantation site with a peak at pregnancy D6, and a shift with primary decidualization to secondary decidualized zones. Using the delayed implantation, the delayed implantation activation, and the artificial decidualization models, we have demonstrated that strong expression of UCHL1 occurred in response to decidualization and estrogen stimulation. These observations suggest that during the early proliferation and differentiation of mouse uterine decidua, UCHL1 expression is up-regulated, and formed an unique intracellular distribution mode. Therefore, we proposed that UCHL1 is involved in decidualization, and possibly in response to estrogen regulation.

UCHL1在几乎所有研究过的模型生物（包括果蝇）的大脑和性腺中都有特异性表达，斑马鱼，两栖动物和哺乳动物，表明其结构和功能具有高度的进化保守性。尽管UCHL1已参与小鼠的精子发生，但在哺乳动物胎盘中的特异性表达仍然难以捉摸。我们以前的工作表明，UCHL1在卵母细胞中高度表达，并参与了小鼠卵巢的卵泡发育。在这里，我们进一步检查了早期自然妊娠期间子宫内膜中UCHL1表达的变化，以动情周期和假性妊娠的不同阶段作为对照。UCHL1基因缺失模型表明，UCHL1蛋白与子宫内膜发育有关，其缺失导致不孕。值得注意的是，我们证明了UCHL1的独特表达模式：子宫内膜的弱表达，蜕膜化的基质细胞在植入位点强烈表达，在妊娠D6达到高峰，并随着初级蜕膜化向次级蜕膜化区域转移。使用延迟植入，延迟植入激活，和人工蜕膜化模型，我们已经证明了UCHL1的强烈表达发生了蜕膜化和雌激素刺激。这些观察结果表明在小鼠子宫蜕膜的早期增殖和分化过程中，UCHL1表达被上调，并形成了独特的细胞内分布模式。因此，我们建议UCHL1参与蜕膜化，并可能参与雌激素调节。使用延迟植入，延迟植入激活和人工蜕膜化模型，我们已经证明了UCHL1的强烈表达发生在蜕膜化和雌激素刺激。这些观察结果表明在小鼠子宫蜕膜的早期增殖和分化过程中，UCHL1表达被上调，并形成了独特的细胞内分布模式。因此，我们建议UCHL1参与蜕膜化，并可能参与雌激素调节。使用延迟植入，延迟植入激活，和人工蜕膜化模型，我们已经证明了UCHL1的强烈表达发生了蜕膜化和雌激素刺激。这些观察结果表明，在小鼠子宫蜕膜的早期增殖和分化过程中，UCHL1表达被上调，并形成了独特的细胞内分布模式。因此，我们建议UCHL1参与蜕膜化，并可能参与雌激素调节。这些观察结果表明，在小鼠子宫蜕膜的早期增殖和分化过程中，UCHL1表达被上调，并形成了独特的细胞内分布模式。因此，我们建议UCHL1参与蜕膜化，并可能参与雌激素调节。这些观察结果表明，在小鼠子宫蜕膜的早期增殖和分化过程中，UCHL1表达被上调，并形成了独特的细胞内分布模式。因此，我们建议UCHL1参与蜕膜化，并可能响应雌激素调节。