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Reproduction Advance Publication first posted online on 27 February 2008

(Reproduction 2008;135:705.)

Reproduction (2008)
DOI: 10.1530/REP-08-0014
Copyright © 2008 Society for Reproduction and Fertility
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RESEARCH

Relaxin and estrogen affect estrogen receptor-{alpha}, vascular endothelial growth factor and relaxin receptor expression in the neonatal porcine uterus and cervix

Wenbo Yan, Joseph Chen, Anne Wiley, Bethany Crean-Harris, Frank Bartol and Carol Bagnell

W Yan, Animal Sciences, Rutgers, the State University of New Jersey, New Brunswick, United States
J Chen, Animal Sciences, Rutgers, the State University of New Jersey, New Brunswick, United States
A Wiley, Animal Sciences, Auburn University, Auburn, United States
B Crean-Harris, Animal Sciences, Auburn University, Auburn, United States
F Bartol, Animal Sciences, Auburn University, Auburn, United States
C Bagnell, Department of Animal Sciences, Rutgers, The State University of New Jersey, New Brunswick, 8901, United States

Correspondence: Carol Bagnell, Email: bagnell{at}aesop.rutgers.edu

Abstract

The porcine female reproductive tract undergoes estrogen receptor (ER) {alpha}-dependent development after birth (postnatal day = PND 0), the course of which can determine adult uterine function. Uterotrophic effects of relaxin (RLX) in the porcine neonate are age-specific and may involve ER activation. Here, objectives were to determine effects of RLX and estrogen administered from birth on uterine and cervical growth and expression of ER{alpha}, vascular endothelial growth factor (VEGF) and the RLX receptor (RXFP1). On PND 0, gilts were treated with the antiestrogen ICI 182,780 (ICI) or vehicle alone and, two hours later, were given estradiol-17β (E) or porcine RLX for two days. Neither RLX nor E affected uterine wet weight or protein content on PND 2. However, RLX, but not E, increased cervical wet weight and protein content when compared to controls. Pretreatment with ICI did not inhibit RLX-stimulated cervical growth. Uterine and cervical ER{alpha} increased in response to RLX, but not E. Both RLX and E increased VEGF in the uterus and cervix on PND 2. Pretreatment with ICI increased VEGF in both tissues and increased RLX-induced cervical VEGF. In the uterus E, but not RLX, increased RXFP1 mRNA. In the cervix, E increased RXFP1 gene expression whereas RLX decreased it. Results indicate that the neonatal uterus and cervix are sensitive to E and RLX and that growth responses to RLX in these tissues differ by PND 2. Effects of RLX on uterine and cervical ER{alpha} and VEGF expression may be important for neonatal reproductive tract development.







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Copyright © 2008 by the Society for Reproduction and Fertility.