ABSTRACT
The functional integrity and cytoarchitectural remodeling of the endometrium is coordinately controlled by the action of steroid hormones and growth factors/ cytokines. The classic bipartite (genomic) model of steroid-target cell interaction involves receptormediated transcriptional activation of target genes in cells to produce major physiological effects some 12-24 hours after hormone treatment (Gronemeyer, 1991). To more clearly define the selective action of hormones on target cells this model has recently been extended to include ligand-receptor-effector schemes (Katzenellenbogen et al., 1996). However, the functional and morphological changes that occur in cultured endometrial cells in response to steroid challenge are too rapid (seconds to a few minutes) to be mediated via the classic genomic pathway (Revelli et al., 1998), and indicate the involvement of signal transduction pathways affiliated with plasma membrane receptors. The existence of a non-classic (nongenomic) steroid response mechanism suggests the potential for cross-talk between steroids and pep tides via the same signaling pathways. The focus of this chapter will be the cross-talk between prolactin (PRL) and progesterone in the regulation of uteroglobin (UG), uteroferrin (UF) and Muc-1 expression in the epithelial cells of the endometrium. Evidence from the UG model that PRL activates a RUSH protein pathway as an alternative to the Jak/Stat pathway supports the idea that PRL may signal through different routes within the same cell.
