Progesterone-action in the decidual mesometrium of pregnancy

The mesometrial decidua is absolutely dependent on progesterone action for its maintenance and growth. Hormone action is mediated by intranuclear progesterone receptors (PR) that regulate target cell gene transcription. In early pregnancy of the rat gene expression is particularly enhanced for regulators of cell cycle progression, growth factors and their cognate receptors; cell cycle arrest proteins are suppressed. Cell survival proteins such as Bcl2 are also up-regulated. These events are associated with abundant expression of PR-A and PR-B isoforms and STAT (signal transducers and activators of transcription) family members. Proliferation of decidual cells no longer occurs after mid-pregnancy despite high levels of circulating progesterone and the decidua begins a slow process of regression, which continues to term. Regression is characterized by an increase in abundance of proteins that promote apoptosis such as p27, Bax and Caspase-3. These late pregnancy changes are associated with a relative increase in PR-C, a third form of the PR molecule, that binds progesterone but probably has limited transcriptional activity. Protein kinase C, which is suppressed by progesterone in early pregnancy, may be a key mediator of these processes.