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Estrogen-Induced Up-Regulation of Androgen Receptor (AR) Expression and Enhancement of AR Nuclear Translocation in Mouse Fallopian Tubes in vivo

Journal article
Authors Linus Ruijin Shao
Karin Ljungström
Birgitta Weijdegård
Emil Egecioglu
Julia Fernandez-Rodriguez
Fu-Ping Zhang
Ann Thurin-Kjellberg
Håkan Billig
Published in Am J Physiol Endocrinol Metab.
Volume 292
Issue 2
Pages 604-614
Publication year 2006
Published at Institute of Biomedicine, Department of Medical and Clinical Genetics
Institute of Neuroscience and Physiology, Department of Physiology
Institute of Clinical Sciences
Pages 604-614
Language en
Subject categories Physiology


Female mice lacking AR display alterations in ovarian and uterine function. However, the biology of AR in the fallopian tube is not fully understood. To gain an insight into potential roles of AR in this tissue, we demonstrated that eCG treatment increased AR expression in a time-dependent manner and subsequent treatment with hCG decreased AR expression in mouse fallopian tubes. This expression pattern was positively associated with 17beta-estradiol and testosterone levels in vivo. Immunohistochemical analysis of fallopian tube epithelial cells revealed that nuclear localization of AR increased in parallel with decreased AR in the cytoplasm following eCG treatment. Moreover, we found that treatment with flutamide upregulated AR expression in immature mice in association with a decrease in serum testosterone levels, whereas the same treatment resulted in downregulation of AR expression in gonadotropin-stimulated mice with concomitant decreases in serum 17beta-estradiol concentrations, suggesting that androgen differs from estrogen in the regulation of AR expression. Furthermore, we demonstrated that DES increased both AR protein expression and nuclear location over a 48-h time course. DHT had rapid effects, with induction of AR expression and translocation at 6 h after injection, but unlike DES it had prolonged efficacy. In addition, we provided direct in vivo evidence that nuclear protein interaction between AR and p21(Cip1), a previously reported AR-regulated gene, was enhanced by gonadotropin stimulation. To our knowledge, this study provides the first demonstration to illustrate that estrogen as a principal regulator may contribute to regulate and activate AR in the fallopian tubes in vivo.

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