ABSTRACT
Many lines of evidence suggest that ovarian steroids affect stromal-epithelial cell interactions within the reproductive tract through paracrine mediators. Very compelling work on this subject has recently been done with steroid receptor knockout mice. Studies in estrogen receptor (ER) alpha knockout mice (Cooke et al., 1998) showed that uterine luminal epithelial proliferation depended on stromal, not epithelial ER, and the results implicated a diffusible mediator (an estromedin), which transfers information from
stroma to epithelium. Similar work in progesterone receptor (PR) knockout mice (Kurita et al., 1998) showed that the suppressive effects of P on estrogen-dependent uterine epithelial DNA synthesis depended on stromal, not epithelial, PR. A P-dependent stromally-derived factor (a progestomedin) may be implicated. In addition, immunocytochemical studies of PR in the human (Lessey et al., 1988) and nonhuman primate (Brenner et al., 1991; Okulicz et al., 1990) endometrium all agree that during the luteal phase, P suppresses PR in the glands, but not the stroma. Yet, P-dependent secretory changes occur in the glands, which further suggests that a stromally-derived, Pdependent progestomedin may play a paracrine role.
