Identification and characterization of uterine transcriptional and translational factors contributing to endocrine disruption of the pregnant and pseudopregnant model phenotype in pigs

Scope and Methods of Study. Embryonic mortality has been demonstrated to occur through endocrine disruption of the uterine environment in the pig. Exogenous estrogen administration to pregnant gilts on days 9 and 10 of pregnancy results in complete embryonic mortality by day 16 of gestation. The current investigation discovered uterine dysfunction caused by early estrogen exposure in pigs through removing conceptus contributions via construction of an endocrine disrupted psuedopregnant pig model. The following study focused on the window of attachment during early gestation in which a significant amount of embryonic mortality occurs. This investigation examined potential mechanisms involved during the window of attachment, and how endocrine disruption within those mechanisms may lead to reduced litter size in swine production.Findings and Conclusions. Successful pregnancy in the pig appears to center around a robust and well defined immune response at the proper time. The current dissertation established four distinct studies which all culminated around proper timing of the vital immune response during days 10 through 18 of early pregnancy in the pig. Additionally, the current study used microarray analysis to demonstrate potential roles estrogen may play in regulating the immune system during this critical time of pregnancy in the pig. Furthermore, all four studies confirmed estrogen's ability to craft mistiming during the uterine window of attachment through transcriptional and translational regulation. These studies have provided a list of potential candidate genes and proteins to further elucidate the mechanism by which early exposure of estrogen terminates pregnancy in the pig.