HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal My Folders Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Fisher, J. S. Articles by Breton, S. Search for Related Content PubMed PubMed Citation Articles by Fisher, J. S. Articles by Breton, S. Agricola Articles by Fisher, J. S. Articles by Breton, S.

Modulation of the Onset of Postnatal Development of H⁺-ATPase-Rich Cells by Steroid Hormones in Rat Epididymis¹

^a Medical Research Council, Human Reproductive Sciences Unit, Edinburgh EH16 4SB, United Kingdom ^b Renal Unit and Program in Membrane Biology, Massachusetts General Hospital, Charlestown, Massachusetts 02129 ^c Department of Medicine, Harvard Medical School, Boston, Massachusetts 02215

Vacuolar type H⁺-ATPase is involved in lumenal acidification of the epididymis. This protein is highly expressed in narrow and clear cells where it is located in the apical pole, and it contributes to proton secretion into the lumen. We have previously shown that in rats, epididymal cells rich in H⁺ATPase appear during postnatal development and reach maximal numbers at 3–4 wk of age. The factors that regulate the appearance of these cells have not been investigated, but androgens, estrogens, or both may be involved. This study examined whether neonatal administration of estrogens (diethylstilbestrol [DES] or ethinyl estradiol) or an antiandrogen (flutamide), or the suppression of androgen production via administration of a GnRH antagonist (GnRHa), was able to alter the appearance of cells rich in H⁺-ATPase in the rat epididymis when assessed at age 25 days. Surprisingly, all of these treatments were able to significantly reduce the number of H⁺-ATPase positive cells; this was determined by immunofluorescence and confirmed by Western blotting. In contrast, neonatal coadministration of DES and testosterone maintained the expression of H⁺-ATPase in the epididymis at Day 25 despite the high level of concomitant estrogen exposure. These findings indicate that androgens, acting via the androgen receptor, are essential for the normal development of epididymal cells rich in H⁺-ATPase, and that treatments that interfere directly or indirectly with androgen production (GnRHa, DES) or action (flutamide, DES) will result in reduced expression of H⁺-ATPase. Our findings do not exclude the possibility that estrogens can directly suppress the postnatal development of cells in the epididymis that are rich in H⁺-ATPase, but if this is the case, this suppression can be prevented by testosterone administration.

¹ This work was supported by grant QLK4-1999-01422 from the European Union to J.F. and by grants HD40793 and DK38452 from the National Institutes of Health (NIH) to S.B. N.P.-S. was supported by NIH NRSA award HD08684.

² Correspondence: Jane Fisher, Medical Research Council, Human Reproductive Sciences Unit, 49 Little France Crescent, Old Dalkeith Rd., Edinburgh EH16 4SB, U.K. FAX: 44 0 131 228 5571; j.fisher{at}hrsu.mrc.ac.uk

This article has been cited by other articles:

				G. I. Gorodeski, U. Hopfer, C. C. Liu, and E. Margles Estrogen Acidifies Vaginal pH by Up-Regulation of Proton Secretion via the Apical Membrane of Vaginal-Ectocervical Epithelial Cells Endocrinology, February 1, 2005; 146(2): 816 - 824. [Abstract] [Full Text] [PDF]

				N. Pastor-Soler, V. Beaulieu, T. N. Litvin, N. Da Silva, Y. Chen, D. Brown, J. Buck, L. R. Levin, and S. Breton Bicarbonate-regulated Adenylyl Cyclase (sAC) Is a Sensor That Regulates pH-dependent V-ATPase Recycling J. Biol. Chem., December 5, 2003; 278(49): 49523 - 49529. [Abstract] [Full Text] [PDF]