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Aquaporin 9 expression in the developing rat epididymis is modulated by steroid hormones

¹ Program in Membrane Biology and Nephrology Division, Center for Systems Biology, Massachusetts General Hospital, 185 Cambridge Street, Suite CPZN 8.204, Boston, Massachusetts 02114, USA
² Harvard Medical School, Boston, Massachusetts 02115, USA
³ Medical Research Council Human Reproductive Sciences Unit, The Queen's Medical Research Institute, Centre for Reproductive Biology, Edinburgh EH16 4TJ, UK

Correspondence should be addressed to S Breton at Program in Membrane Biology and Nephrology Division, Center for Systems Biology, Massachusetts General Hospital; Email: breton.sylvie{at}mgh.harvard.edu

N M Pastor-Soler is now at the Renal-Electrolyte Division, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15261, USA

Fluid and solute transport across the epithelium of the male excurrent duct is important for sperm maturation and storage. Aquaporin 9 (AQP9), which allows permeation of water and neutral solutes, is abundant throughout the male reproductive tract, where it is expressed at the apical membrane of rat epididymal principal cells as early as at 1 week of age. We evaluated the effect of neonatal exposure to: 1) a GNRH antagonist (GNRHa); 2) diethylstilbestrol (DES); 3) ethinyl estradiol (EE); 4) DES plus testosterone (DES+TE); and 5) the anti-androgen flutamide on AQP9 expression in the epididymis of peripubertal rats. Control groups received the vehicle alone. In 25-day-old rats, quantification of the mean pixel intensity of immunofluorescence-stained sections showed a significant decrease in AQP9 staining in the apical membrane of epididymal principal cells after treatments with GNRHa, DES, or flutamide, compared to controls. These results were confirmed by western blotting. While EE induced a marked decrease in AQP9 levels by western blotting, the decrease in AQP9-associated fluorescence was not significant compared to controls. DES+TE-treated rats showed levels of AQP9 protein similar to controls, indicating maintenance of AQP9 expression by testosterone treatment in the presence of DES. Our data show that expression of AQP9 in the developing rat epididymis is downregulated by neonatal DES, GNRHa, EE, and flutamide, and that the effects mediated by estrogens can be prevented by testosterone administration.