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Updated: Nov 5, 2025

Isolation of Mouse Endometrial Epithelial and Stromal Cells for In Vitro Decidualization
Published on: March 2, 2017
Usp22 is expressed in mouse uterus during early pregnancy and involved in endometrial stromal cell decidualization
Yaqin Wang1, Yue Gao1, Chan Zhou2
1Reproductive 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.
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.
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.
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