help button home button Endocrine Society Endocrinology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Copyright Permission
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Cooke, P. S.
Right arrow Articles by Cunha, G. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Cooke, P. S.
Right arrow Articles by Cunha, G. R.

Endocrinology, Vol 121, 2153-2160, Copyright © 1987 by Endocrine Society


ARTICLES

Androgen dependence of growth and epithelial morphogenesis in neonatal mouse bulbourethral glands

PS Cooke, PF Young and GR Cunha
University of California, San Francisco 94143.

The early development of the mouse bulbourethral gland (BUG) and the role of testosterone (T) in the normal growth and epithelial morphogenesis of this male accessory sex gland were examined. The mouse BUG differentiates from the urogenital sinus on day 17 of gestation (vaginal plug = day 0; birth = day 19), and initially consists of a solid epithelial rudiment encased in a large condensed capsular mesenchyme. The epithelium begins to branch and canalize on day 1 postnatally, and the branches enlarge and become more numerous on days 2 and 3. On day 4, secondary branches appear, and by day 6, the epithelium has become extensively arborized and almost fills the mesenchymal capsule. The BUG increases 3.9-fold in DNA content from day 0 (day of birth) to day 6 postnatally; the epithelium grows proportionately more than the mesenchyme during this period (12-fold vs. 2.3-fold). Growth of BUGs in mice castrated at birth or castrated and then treated with cyproterone acetate, an antiandrogen, over the first 6 days of life was reduced by 80%, but not abolished. Thus, the growth of the BUG is partially independent of androgens during early neonatal life. However, morphogenesis of the BUG epithelium is totally abolished in neonatally castrated mice. T replacement given to neonatally castrated mice during days 0-6 restored development to normal. T injections also reinitiated growth and morphogenesis in developmentally retarded BUGs from 6-day-old neonatally castrated mice. The partial dependence of the neonatal BUG on androgens for growth is similar to that seen in the prostate, which is also derived from the urogenital sinus. In contrast to the prostate, where neonatal castration reduces but does not abolish epithelial morphogenesis, androgen deprivation completely abolished epithelial morphogenesis in the neonatal BUG. (Endocrinology 121: 2153-2160, 1987).


This article has been cited by other articles:


Home page
Genes Dev.Home page
R. Bhatia-Gaur, A. A. Donjacour, P. J. Sciavolino, M. Kim, N. Desai, P. Young, C. R. Norton, T. Gridley, R. D. Cardiff, G. R. Cunha, et al.
Roles for Nkx3.1 in prostate development and cancer
Genes & Dev., April 15, 1999; 13(8): 966 - 977.
[Abstract] [Full Text]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals
Copyright © 1987 by The Endocrine Society