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Am J Physiol Endocrinol Metab (September 11, 2007). doi:10.1152/ajpendo.00384.2007
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Submitted on June 19, 2007
Accepted on September 3, 2007

Dynamic regulation of estrogen receptor alpha isoform expression in the mouse fallopian tube: mechanistic insight into estrogen-dependent production and secretion of insulin-like growth factors

Ruijin Shao1*, Emil Egecioglu1, Birgitta Weijdegard1, John J Kopchick2, Julia Fernandez-Rodriguez3, Niklas Andersson4, and Hakan Billig1

1 Department of Physiology/Endocrinology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at Gothenburg University, Gothenburg, Sweden
2 Konneker Research Laboratories,, Edison Biotechnology Institute, Ohio University, Athens, Ohio, United States
3 Centre for Cellular Imaging, Core facilities, The Sahlgrenska Academy at Gothenburg University, Gothenburg, Sweden
4 Division of Endocrinology, Department of Internal Medicine, The Sahlgrenska Academy at Gothenburg University, Gothenburg, Sweden

* To whom correspondence should be addressed. E-mail: ruijin.shao{at}fysiologi.gu.se.

Here we provide for the first time insight into the less studied ER{alpha} isoforms which mediate estrogen-dependent production and secretion of insulin-like growth factors in vivo. Firstly, Western blot studies revealed that three ER{alpha} isoforms were expressed in mouse fallopian tubes. Subsequent immunohistochemical analysis showed that ER{alpha} was detected in all cell types, whereas ER{beta} was mainly localized in the ciliated epithelial cells. Secondly, ER{alpha} isoform levels were dramatically down-regulated in mouse fallopian tubes by treatment with E2 or PPT, an ER{alpha} agonist, in a time-dependent manner. Thirdly, the presence of ICI 182,780 blocked the E2- or PPT- induced down-regulation of tubal ER{alpha} isoform expression in mice. However, alteration of ER{alpha} immunoreactivity following ICI 182,780 treatment was only detected in the epithelial cells of ampullary region. Fourthly, changes in ER{alpha} isoform expression were found to be coupled to multiple E2 effects on tubal growth, protein synthesis and secretion in mouse fallopian tube tissues and fluid. In particular, E2 exhibited positive regulation of IGF-I and IGF-II protein levels. Finally, using growth hormone receptor (GHR) gene disrupted mice, we showed that the regulation of IGF production was independent of GH induced GHR signaling in mouse fallopian tubes in vivo. These data, together with previous studies from our laboratory, suggest that the long-term effects of estrogen agonist promote IGF synthesis and secretion in mouse tubal epithelial cells and fallopian tube fluid via stimulation of ER{alpha}.




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