Reproductive Medical Center, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China; Hubei Clinic Research Center for Assisted Reproductive Technology and Embryonic Development, Wuhan, Hubei 430060, China.
Reproductive Medical Center, The First Affiliated Hospital of Xiamen University, Xiamen, Fujian 361005, China; Fujian Provincial Key Laboratory of Reproductive Health Research, Medical College of Xiamen University, Xiamen, Fujian 361005, China.
Cells Dev. 2021 Jun;166:203681. doi: 10.1016/j.cdev.2021.203681. Epub 2021 Apr 30.
While decidualization is essential for embryo implantation in the context of a normal pregnancy, the molecular basis for this process remains poorly understood. Ubiquitin-specific protease 22 (Usp22), one of the deubiquitinating enzymes, is an important regulator of tumor progression and knocking out this gene in mice results in placental vascular dysplasia and embryonic lethality. In this study, we first demonstrated that Usp22 is spatiotemporally expressed in the mouse peri-implantation uterus. Under artificial decidualization, Usp22 upregulation was detected in both in vivo and in vitro. Progesterone treatment could stimulate Usp22 expression in mouse endometrial stromal cells through progesterone/progesterone receptor (PR) pathway, which is inhibited by PR antagonist. The downregulation of Usp22 within mouse endometrial stomal cells by shRNA impaired their ability to proliferate and undergo decidualization. Taken together, these results suggest that Usp22 is involved in uterine stromal decidualization in mice.
虽然蜕膜化对于正常妊娠中的胚胎着床至关重要，但这一过程的分子基础仍知之甚少。泛素特异性蛋白酶 22（Usp22）是去泛素化酶之一，是肿瘤进展的重要调节剂，敲除该基因会导致胎盘血管发育不良和胚胎致死。在这项研究中，我们首先证明 Usp22 在小鼠着床前子宫中具有时空表达。在人工蜕膜化下，体内和体外均检测到 Usp22 的上调。孕激素通过孕激素/孕激素受体（PR）途径刺激小鼠子宫内膜基质细胞中 Usp22 的表达，该途径可被 PR 拮抗剂抑制。shRNA 下调小鼠子宫内膜基质细胞中的 Usp22 会损害其增殖和蜕膜化的能力。综上所述，这些结果表明 Usp22 参与了小鼠子宫基质的蜕膜化。
