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1 Department of Physiology/Endocrinology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at Göteborg University, Göteborg, Göteborg, Sweden
2 Department of Physiology/Endocrinology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at Göteborg University, Göteborg, Göteborg, Sweden; Göteborg, Göteborg, Sweden
3 Department of Reproductive Medicine, Sahlgrenska University Hospital, Göteborg University, Göteborg, Göteborg, Sweden; Department of Physiology/Endocrinology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at Göteborg University, Göteborg, Göteborg, Sweden
4 Göteborg, Göteborg, Sweden; Department of Physiology/Endocrinology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at Göteborg University, Göteborg, Göteborg, Sweden
5 Swegene Centre for Cellular Imaging, Göteborg University, Göteborg, Göteborg, Sweden
6 Department of Physiology, Institute of Biomedicine, University of Helsinki, Helsinki, Helsinki, Finland
7 Göteborg, Göteborg, Sweden; Department of Reproductive Medicine, Sahlgrenska University Hospital, Göteborg University, Göteborg, Göteborg, Sweden
* To whom correspondence should be addressed. E-mail: ruijin.shao{at}fysiologi.gu.se.
To gain an insight into the potential roles of AR in the fallopian tubes, we demonstrate for the first time that equine chorionic gonadotropin (eCG) treatment increases AR expression in a time-dependent manner and that subsequent treatment with human (h)CG decreases AR expression in mouse fallopian tubes. Immunohistochemical analysis of fallopian tube epithelial cells shows that nuclear localization of AR increases in parallel with decreased AR in the cytoplasm following eCG treatment. Moreover, we found that treatment with flutamide up-regulated AR expression in immature mice in association with a decrease in serum testosterone levels, whereas the same treatment resulted in down-regulation of AR expression in gonadotropin-stimulated mice with a concomitant decreases in serum 17
-estradiol concentrations. In order to determine which steroid hormone affected AR accumulation and translocation in mouse fallopian tubes, we demonstrate that treatment with diethylstilbestrol increased both AR protein expression and nuclear location over a 48-h time course. Dihydrotestosterone had rapid effects, with induction of AR expression and translocation at 6 h after injection. Neither AR expression nor translocation was affected by progesterone. Furthermore, we provide direct in vivo evidence that nuclear protein interaction between AR and p21Cip1, a previous reported AR-regulated gene, is enhanced by gonadotropin stimulation in mouse fallopian tubes. To our knowledge, this study provides the first demonstation to illustrate that estrogen, as a principal regulator, may contribute to increase AR protein expression and cause nuclear translocation in the fallopian tubes in vivo.
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