Document Detail

Increased levels of clusterin (SGP-2) mRNA and protein accompany rat ventral prostate involution following finasteride treatment.
MedLine Citation:
PMID:  11054633     Owner:  NLM     Status:  MEDLINE    
Finasteride is a well-known inhibitor of the prostatic enzyme 5 alpha-reductase type 2 which prevents conversion of testosterone into 5 alpha-dihydrotestosterone, the active intraprostatic androgen, which causes prostate involution through a combination of cell atrophy and cell death. The drug is widely used to improve symptoms of benign prostatic hyperplasia in man. Clusterin, a glycoprotein which is generally up-regulated under conditions inducing cell atrophy or organ involution, is produced at a high level in the regressing rat ventral prostate following androgen ablation. According to several authors, clusterin does not respond to finasteride treatment, suggesting a different action of testosterone and 5 alpha-dihydrotestosterone. We show here that, under our conditions, finasteride was capable of inducing production of both clusterin mRNA and protein in the rat ventral prostate. In fact, by using different and converging techniques, such as Northern hybridization, in situ hybridization histochemistry and immunohistochemistry, we were able to show a strong induction of the clusterin gene in the epithelial cell population of the gland. The response to finasteride, which was similar to that seen with castration, occurred with a delay of a few days. In situ and immunohistochemistry experiments indicated that both orchidectomy and finasteride administration resulted in increased transition of the epithelial cells from the columnar to the cuboidal (atrophic) shape, and this was accompanied by an increased intensity of the signal for clusterin. Thus, it appears that induction of clusterin is part of the molecular process leading to prostate involution caused by either orchidectomy or finasteride administration.
S Astancolle; G Guidetti; C Pinna; A Corti; S Bettuzzi
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Journal of endocrinology     Volume:  167     ISSN:  0022-0795     ISO Abbreviation:  J. Endocrinol.     Publication Date:  2000 Nov 
Date Detail:
Created Date:  2000-12-15     Completed Date:  2000-12-15     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0375363     Medline TA:  J Endocrinol     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  197-204     Citation Subset:  IM    
Dipartimento di Scienze Biomediche, Università di Modena e Reggio Emilia, Via G. Campi 287, 41100 Modena, Italy.
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MeSH Terms
Blotting, Northern
Enzyme Inhibitors / pharmacology*
Finasteride / pharmacology*
Gene Expression Regulation / drug effects*
Glycoproteins / genetics*,  metabolism
Immunoenzyme Techniques
In Situ Hybridization
Molecular Chaperones*
Prostate / drug effects*,  metabolism,  pathology
RNA, Messenger / genetics
Rats, Sprague-Dawley
Testosterone 5-alpha-Reductase / antagonists & inhibitors
Reg. No./Substance:
0/Clusterin; 0/Enzyme Inhibitors; 0/Glycoproteins; 0/Molecular Chaperones; 0/RNA, Messenger; 98319-26-7/Finasteride; EC 5-alpha-Reductase

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