Document Detail

Androgen action in the epididymis.
MedLine Citation:
PMID:  21764895     Owner:  NLM     Status:  MEDLINE    
Androgens are responsible for maintaining epididymal structure and functions. However, little is known about how androgen action is mediated and the mechanisms underlying the restoration of the integrity of epididymal cells after androgen deprivation. We first provide an overview of what is known about androgen action in this tissue and then present data on the initial and sequential roles of androgens in altering cellular architecture and function in an androgen-deprived condition. Using morphometric analysis and the rat model, we identified changes in epithelial cell height and lumen diameter, as well as in the numbers of proliferating cells in different regions and at various time points after androgen withdrawal and replacement. The sequence of gene activation or suppression that occurred in the androgen-deprived tissue was examined upon the readministration of the 2 active metabolites of testosterone, dihydrotestosterone (DHT) and estradiol. Although few genes were regulated by estradiol, many were affected by DHT. Epidermal growth factor (EGF) and insulinlike growth factor-1 (IGF1) appear to play an important role in the early response pathway activated by DHT because of their function in the regulation of the expression of many other genes. The intracellular signaling pathway involved in mediating the action of androgen in restoring epididymal epithelial cell integrity was investigated using the PC-1 epididymal cell line. IGF1 and EGF receptors were found to be important mediators of androgen receptor-mediated activation of the MAPK/ERK pathways. Together, these studies provide a greater understanding of the mechanisms of androgen action in the epididymis.
Bernard Robaire; Mahsa Hamzeh
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review     Date:  2011-07-15
Journal Detail:
Title:  Journal of andrology     Volume:  32     ISSN:  1939-4640     ISO Abbreviation:  J. Androl.     Publication Date:    2011 Nov-Dec
Date Detail:
Created Date:  2011-10-05     Completed Date:  2012-02-13     Revised Date:  2012-03-02    
Medline Journal Info:
Nlm Unique ID:  8106453     Medline TA:  J Androl     Country:  United States    
Other Details:
Languages:  eng     Pagination:  592-9     Citation Subset:  IM    
Department of Pharmacology & Therapeutics, McGill University, 3655 Promenade Sir William Osler, Montreal, Quebec, Canada.
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MeSH Terms
Androgens / metabolism*
Cell Proliferation
Epidermal Growth Factor / metabolism
Epididymis / metabolism*
Estradiol / metabolism
Gene Expression Regulation
Insulin-Like Growth Factor I / metabolism
MAP Kinase Signaling System
Receptor, Epidermal Growth Factor / metabolism
Receptor, IGF Type 1 / metabolism
Receptors, Androgen / metabolism
Grant Support
MOP-86735//Canadian Institutes of Health Research
Reg. No./Substance:
0/Androgens; 0/Receptors, Androgen; 50-28-2/Estradiol; 62229-50-9/Epidermal Growth Factor; 67763-96-6/Insulin-Like Growth Factor I; EC, Epidermal Growth Factor; EC, IGF Type 1

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