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Differences in Prolactin Receptor (PRLR) in Mouse and Human Fallopian Tubes: Evidence for Multiple Regulatory Mechanisms Controlling PRLR Isoform Expression in Mice¹

Department of Physiology/Endocrinology,⁴ Institute of Neuroscience and Physiology, The Sahlgrenska Academy at Gothenburg University, SE-41390 Gothenburg, Sweden Center for Cellular Imaging,⁵ Core Facilities, The Sahlgrenska Academy at Gothenburg University, SE-41390 Gothenburg, Sweden Institut National de la Santé et de la Récherche Médicale,⁶ Unité 845, Centre de Recherche "Croissance et Signalisation," Equipe "PRL, GH et Tumeurs," F-75015 Paris, France Faculté de Médecine,⁷ Université Paris Descartes, F-75015 Paris, France Department of Clinical Science,⁸ Lund University, CRC, University Hospital MAS, SE-20502 Malmö, Sweden

ABSTRACT

The anterior pituitary-derived hormone prolactin (PRL) signals through the PRL receptor (PRLR) and is important for female reproductive function in mammals. In contrast to the extensive studies of PRLR expression and regulation in human and mouse ovary and uterus, the mechanisms controlling the regulation of PRLR isoform expression in the fallopian tube are poorly understood. Because dynamic interaction of hormonal signaling in gonadal tissue and the pituitary or in gonadal tissues themselves in mammals suggests endocrine or paracrine regulation of PRLR expression, we questioned whether differential regulation of PRLR isoforms by PRL ovarian-derived estrogen (E₂) and progesterone (P₄) exists in the fallopian tube and pituitary of prepubertal female mice. Western blot analysis showed distinct molecular separation of PRLR isoforms in mouse and human fallopian tubes, and cellular localization was found in mouse and human tubal epithelia but not in mouse tubal smooth muscle cells. These data support the concept of an isoform- and cell type-specific expression of PRLR in human and mouse fallopian tubes. Moreover, expression of the long form of PRLR decreased after PRL treatment and increased after blockage of endogenous PRL secretion by bromocriptine (an inhibitor of PRL secretion) in a time-dependent manner in mouse fallopian tube. The opposite regulation was observed in the pituitary. Treatment with exogenous E₂ or P₄ led to changes in PRLR expression in the fallopian tube similar to those of PRL treatment. However, E₂ and P₄ did not affect PRLR expression in the pituitary. Estrogen had no effect on the long form of PRLR expression, whereas P₄ regulated the long form of PRLR in the fallopian tube, as did PRL. Taken together, the data from our comparative study provide evidence that PRLR can be regulated by an interplay of two different mechanisms, PRL or ovarian steroid hormones independently or in combination in a tissue-specific manner. Furthermore, we found that ovarian steroid hormones selectively suppress the expression of PRLR isoforms in mouse fallopian tubes. These findings may contribute to our understanding of the mechanisms controlling PRLR isoform expression in the fallopian tube (in addition to ovary and uterus), with implications for female reproduction.

estradiol, fallopian tube, ovarian steroid hormones, oviduct, pituitary, prolactin, prolactin receptor, prolactin receptor isoforms

³These authors contributed equally to this work.

¹Supported by Svenska Sällskapet för Medicinsk Forskning, Sahlgrenska Academy Research Council, Göteborgs Läkaresällskap, and Fred G. and Emma E. Kanolds Stiftelse, Hjalmar Svenssons Research Foundation to R.S.; by Rådman and Fru Colliander, Emil and Maria Palm, and Eva and Oscar Ahréns Research Foundations to M.N.; and by grant 10380 from the Swedish Medical Research Council to H.B.

Correspondence: ²FAX: 46 31 7733512; e-mail: ruijin.shao{at}fysiologi.gu.se

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