MCM2 mediates progesterone-induced endometrial stromal cell proliferation and differentiation in mice
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Uterine decidualization characterized by stromal cell proliferation and differentiation is critical to the establishment of pregnancy in many species. Progesterone is a key factor in regulating endometrial cell decidualization, however, the molecular basis involved in mediating the effects of progesterone during decidualization remains largely unknown. We report here that the DNA replication licensing factor MCM2, one of the conserved set of six-related proteins (MCM complex: MCM2–7) essential for eukaryotic DNA replication, is dynamically expressed in both proliferative and differentiated stromal cells during mouse periimplantation uterus. Applying PR-knockout mouse model and pharmacological strategy, we further found that the expression of Mcm2 is induced by progesterone action in the mouse uterine stroma. Employing a primary cell culture system, we further demonstrated that siRNA-mediated silencing of MCM2 arrests the cell cycle at G1–S transition during stromal cell proliferation. Moreover, the downregulation of Mcm2 could also compromise stromal cell differentiation. Collectively, our studies uncovered the role of a unique DNA replication licensing molecule MCM2 in mediating Progesterone-induced stromal cell decidualization in mouse uterus.
KeywordsMcm2 Uterine stroma Decidualization S-phase Progesterone
This work was supported in parts by the National Basic Research Program of China (2011CB944400 to H.W.) and the National Natural Science Foundation (81130009 and 81330017 to H.W. and to 31471106 to S.Z.).
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Conflict of interest
The authors declared that they have no conflict of interests.
- 47.J.M. Sroga, X. Ma, S.K. Das, Developmental regulation of decidual cell polyploidy at the site of implantation. Front. Biosci. (Sch. Ed.). 4, 1475–1486 (2012)Google Scholar
- 48.D.D. Carson, Embryo implantation: molecular, cellular and clinical aspects (Springer Science & Business Media, New York, 2013)Google Scholar