Early uterine development in pigs

The capacity of pig uterine tissues to recognize and respond to maternal and conceptus signals determines whether pregnancy can be established and defines the environment in which embryonic and fetal growth occur. Limits of uterine capacity may be defined genetically. However, the extent to which functional uterine capacity approaches genetic potential may be determined, in part, by the success of organizational events associated with growth, morphogenesis and cytodifferentiation of uterine tissues. It is important, therefore, that these events be identified and evaluated with respect to their potential effect on adult uterine function. Histogenesis of the pig uterus begins prenatally, but is completed postnatally. Transformation of the uterine wall from histoarchitectural infancy to maturity occurs between birth and day 120. Morphogenetic events characteristic of the first 60 days of neonatal life proceed normally in gilts ovariectomized at birth. These events include appearance and proliferation of uterine glands, development of endometrial folds, and growth of the myometrium. Endometrial development during this period involves alterations in patterns of epithelial and stromal DNA synthesis, coordinated changes in the distribution and biosynthesis of extracellular matrix glycosaminoglycans and cell surface glycoconjugates, and specific alterations in patterns of uterine protein secretion. The ovary-independent, spatially coordinated nature of these events suggests that neonatal uterine development is regulated locally via dynamic cell-cell and cell-extracellular matrix interactions. The extent to which such potentially critical interactions must be preserved to ensure developmental success remains unknown. However, the normal pattern of ovary-independent cellular and molecular events associated with development of the uterine wall was disrupted by treating neonatal gilts with oestradiol valerate, and daily administration of oestrogen to gilts from birth to day 13 did not affect ovulation rate, but did reduce embryonic survival by 22% on day 45 of gestation in adults that were exposed to oestrogen neonatally. These observations support the idea that some organizational events associated with development of the neonatal uterine wall must be allowed to proceed without interruption to ensure that adult uterine function is not compromised. Efforts to identify specific developmental determinants of uterine capacity may be facilitated by examining the consequences of xenobiotically induced interruption of uterine development on adult uterine function. Such studies may also contribute to identification of uterine factors affecting embryonic survival and fetal growth.