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A major decidualization regulator is progesterone (P). P is thought to be converted to a ligand for the PR. In this study, we have studied the role of another uterine-gland-specific mediator of decidualization, insulin-like growth factor (IGF)-I and -II. IGF-I and -II are important mediators of uterine decidualization, but little is known about the regulatory mechanism of this process. The role of P and IGF in mediating decidualization was studied by gene expression analysis and the generation and characterization of IGF receptor knockout (igf1r -/-) mice. Treatment of uterine stromal cells (ST) with IGF-I increased cyclin D1 and p21(cip1) and decreased cyclin D3 and RB expression, cyclin B1 and PCNA. The effects of IGF-I were mimicked by the active form of P, whereas the inactive form had no effect. Insulin like growth factor binding protein (IGFBP)-2, a negative regulator of IGF action, attenuated the effect of IGF-I, whereas the active form of P induced IGFBP-2 expression and delayed the action of IGF-I. The effects of IGF-II on stromal cells were very similar to those of IGF-I, and the effects of P were again mimicked by the active form, whereas the inactive form had no effect. Because P induces IGFBP-2, we performed loss of function studies with IGFBP-
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