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Journal of Endocrinology (2009) 202, 153-166       DOI: 10.1677/JOE-08-0486
© 2009 Society for Endocrinology
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Tissue-specific regulation of porcine prolactin receptor expression by estrogen, progesterone, and prolactin

 Josephine F Trott1,2, Katherine C Horigan1, Julia M Gloviczki1,2, Kristen M Costa1, Bradley A Freking3, Chantal Farmer4, Kanako Hayashi5, Thomas Spencer6, Joseph E Morabito1 and Russell C Hovey1,2

1 Lactation and Mammary Gland Biology Group, Department of Animal Science, The University of Vermont, 570 Main Street, Burlington, Vermont 05405, USA
2 Department of Animal Science, University of California, 2145 Meyer Hall, 1 Shields Avenue, Davis, California 95616, USA
3 US Meat Animal Research Center, PO Box 166, Clay Center, Nebraska 68933, USA
4 Agriculture and Agri-Food Canada, PO Box 90, Lennoxville STN, Sherbrooke, Quebec, Canada J1M 1Z3
5 Department of Physiology, Southern Illinois University School of Medicine, 1135 Lincoln Drive, Carbondale, Illinois 62901, USA
6 Department of Animal Science, Center for Animal Biotechnology and Genomics, Texas A&M University, College Station, Texas 77843, USA

(Correspondence should be addressed to R C Hovey at Department of Animal Science, University of California; Email: rchovey{at}ucdavis.edu)

Prolactin (PRL) acts through its receptor (PRLR) via both endocrine and local paracrine/autocrine pathways to regulate biological processes including reproduction and lactation. We analyzed the tissue- and stage of gestation-specific regulation of PRL and PRLR expression in various tissues of pigs. Abundance of pPRLR-long form (LF) mRNA increased in the mammary gland and endometrium during gestation while in other tissues it remained constant. There was a parallel increase in the abundance of the pPRLR-LF protein in the mammary gland and endometrium during gestation. We determined the hormonal regulation of pPRLR-LF mRNA expression in various tissues from ovariectomized, hypoprolactinemic gilts given combinations of the replacement hormones estrogen (E2), progestin (P), and/or haloperidol-induced PRL. Abundance of pPRLR-LF mRNA in kidney and liver was unaffected by hormone treatments. Expression of uterine pPRLR-LF mRNA was induced by E2 whereas the effect of E2 was abolished by co-administering P. The expression of pPRLR-LF mRNA in the mammary gland stroma was induced by PRL, whereas E2 induced its expression in the epithelium. In contrast to these changes in pPRLR expression, pPRL expression was relatively constant and low during gestation in all tissues except the pituitary. Taken together, these data reveal that specific combinations of E2, P, and PRL differentially regulate pPRLR-LF expression in the endometrium and mammary glands, and that the action of PRL on its target tissues is dependent upon pPRLR-LF abundance more so than the local PRL expression.






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