Journal of Andrology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Published-Ahead-of-Print November 8, 2005, DOI:10.2164/jandrol.05114

This Article
Right arrow Author Manuscript (PDF)
Right arrow All Versions of this Article:
27/2/225    most recent
Author Manuscript (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
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
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Turner, T. T.
Right arrow Articles by Tomsig, J. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Turner, T. T.
Right arrow Articles by Tomsig, J. L.

Sonic hedgehog pathway inhibition alters epididymal function as assessed by the development of sperm motility

Terry T. Turner *, Hyun J. Bang , Sharon A. Attipoe , Daniel S. Johnston , and Jose L. Tomsig

* To whom correspondence should be addressed. E-mail: ttt{at}virginia.edu.

The sonic hedgehog (Shh) signaling pathway plays a role in pattern orientation in the developing embryo and has been shown to be required for development of the prostate and external genitalia. Recent evidence has shown that important elements of the shh pathway are also expressed in the adult mouse epididymis at both the gene and protein level. The objective of the present investigation was to refine the expression pattern of Shh in the mouse epididymis and to determine if the Shh pathway is important for epididymal function vis-à-vis sperm maturation. The former was achieved by microarray analysis of Shh expression all segments of the mouse epididymis, and the latter was determined by 14 d administration of cyclopamine, a Shh pathway inhibitor, followed by a microassay for the activation and duration of cauda epididymal sperm motility. Shh pathway inhibition was monitored by semi-quantitative RTPCR for expression of epididymal Gli1 and Gli3. The Gli family of transcription factors are commonly activated and regulated by Shh pathway activation. Cyclopamine treatment reduced Gli1 expression by 61% and initiation of cauda sperm motility by 50%. Gli3 expression was reduced by approximately 50%. Subsequent cluster analysis using the microarray data on epididymal gene expression highlighted several potential target genes for the Shh pathway, the most prominent of which is prostaglandin D2 synthase. These results indicate that an operating shh pathway is important in the murine epididymis for the development of sperm motility and implies a role for shh signaling in adult epididymal function.




This article has been cited by other articles:


Home page
 Toxicol SciHome page
R. J. Lipinski, P. R. Hutson, P. W. Hannam, R. J. Nydza, I. M. Washington, R. W. Moore, G. G. Girdaukas, R. E. Peterson, and W. Bushman
Dose- and Route-Dependent Teratogenicity, Toxicity, and Pharmacokinetic Profiles of the Hedgehog Signaling Antagonist Cyclopamine in the Mouse
Toxicol. Sci., July 1, 2008; 104(1): 189 - 197.
[Abstract] [Full Text] [PDF]

Home page
 J AndrolHome page
T. T. Turner
De Graaf's Thread: The Human Epididymis
J Androl, May 1, 2008; 29(3): 237 - 250.
[Abstract] [Full Text] [PDF]

Home page
 Biol. Reprod.Home page
J. L. Tomsig, S. Usanovic, and T. T. Turner
Growth Factor-Stimulated Mitogen-Activated Kinase (MAPK) Phosphorylation in the Rat Epididymis Is Limited by Segmental Boundaries
Biol Reprod, October 1, 2006; 75(4): 598 - 604.
[Abstract] [Full Text] [PDF]

Home page
 J AndrolHome page
J. L. Tomsig and T. T. Turner
Growth Factors and the Epididymis
J Androl, May 1, 2006; 27(3): 348 - 357.
[Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Copyright © 2005 by The American Society of Andrology.