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RESEARCH |
1 Department of Animal Sciences, Rutgers, The State University of New Jersey, New Brunswick, New Jersey 08901, USA, 2 Department of Animal and Dairy Sciences, Mississippi State University, Mississippi State, Mississippi 39762, USA and 3 Department of Animal Sciences, Cellular and Molecular Biosciences Program, Auburn University, Auburn, Alabama 36849, USA
Correspondence should be addressed to C A Bagnell; Email: bagnell{at}aesop.rutgers.edu
While uterotrophic effects of relaxin are well documented, the mechanism through which relaxin promotes uterine growth is incompletely understood. Studies in rats suggest that relaxin-stimulated uterine edema depends on estrogen receptor (ER) activation. Here, neonatal pigs were used to investigate the interaction between relaxin and ER signaling pathways. Gilts were treated either at birth (postnatal day (PND) 0) (study 1) before the onset of endometrial ER
expression, or on PND 12 (study 2) after the onset of ER
expression. In study 1, gilts were treated with estradiol-17ß or porcine relaxin for two days and uteri were collected on PND 2. In study 2, PND 12 gilts were treated with a single injection of the ER antagonist ICI 182,780 (ICI) or vehicle. Two hours later, gilts were given either estradiol-17ß or porcine relaxin for two days. When administered for two days from birth (study 1), neither estradiol-17ß nor relaxin affected uterine weight or protein content. However, uterine luminal epithelial height was greater in relaxin- than in vehicle-treated gilts. In contrast, in study 2, both estradiol and relaxin increased uterine weight, protein content and uterine luminal epithelial height on PND 14. These effects were inhibited by pre-treatment with ICI in both estradiol- and relaxin-treated gilts. The results indicate that uterotrophic effects of relaxin in the neonatal pig are related to age and to both the relative presence and state of activation of the ER system in developing uterine tissues between birth and PND 14.
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