In that study, appearance of endometrial glands was associated with a dramatic and specific increase in [methyl-3H] thymidine labeling by GE cells, whereas LE labeling actually decreased. The fact that endometrial GE cells develop ER before LE cells in the neonatal porcine endometrium is in contrast to patterns reported for the mouse and rat. However, a positive temporal relationship does exist between the appearance of new endometrial glands, onset of DNA synthesis by GE, and development of ER-positive phenotype in GE cells. This pattern is similar to that observed in rodents. buy ampicillin
Developmental relationships described here suggest that the ER is required mechanistically for normal uterine wall development and, in particular, for proliferation of endometrial glands. In this regard, elegant data have come from studies of ER knockout (ERKO) mice, created to be functionally ER negative. Uteri in ERKO mice are hypoplastic, but they contain all characteristic cell types in reduced proportions. Thus, a functional ER system is not essential for uterine organogenesis but is essential for normal uterine growth in the mouse. Using tissue separation/recombination techniques with wild-type (ER positive) and ERKO (ER negative) uterine stroma and epithelium, mitogenic effects of estradiol on uterine epithelium were shown to require stromal but not epithelial ER. However, both stromal and epithelial ER were required for estradiol-induced uterine epithelial secretory protein production. Broadly, these data can be interpreted to suggest that stromal ER are required to facilitate proliferation of endometrial cells, while epithelial and stromal ER are required to facilitate differentiative events necessary for morphogenetic and cytodifferentiative processes that, together, ensure success of endometrial growth and functional organization.