Document Detail

Differential effects of GnRH and androgens on Cres mRNA and protein in male mouse anterior pituitary gonadotropes.
MedLine Citation:
PMID:  16837735     Owner:  NLM     Status:  MEDLINE    
The Cres gene defines a new subgroup in the family 2 cystatins of cysteine protease inhibitors. However, unlike typical cystatins, CRES does not inhibit cysteine proteases but rather inhibits the serine protease prohormone convertase 2, an enzyme with roles in proprotein processing in the neuroendocrine system. Cres is expressed in the gonadotropes and colocalizes with LHbeta, suggesting a role in the regulation of gonadotrope secretion. Our present studies were carried out to examine the regulation of Cres mRNA and protein expression by GnRH and steroid hormones, thus providing clues regarding its role in gonadotropes. Castration profoundly reduced Cres mRNA, while replacement with estradiol (E(2)), testosterone (T), or dihydrotestosterone (DHT) further decreased Cres, suggesting negative regulation by GnRH or steroid hormones. The administration of Antide, a GnRH antagonist, resulted in a 3-fold increase in Cres mRNA, supporting a negative regulation by GnRH. Because all hormonal manipulations in vivo resulted in alterations in steroid hormones, organ culture was used to assess the effects of GnRH independent of steroids. Mouse pituitaries cultured in the absence of GnRH or steroids showed high Cres mRNA levels, while DHT or E(2) resulted in decreases of 25% and 68%, respectively. However, an 85% decrease in Cres mRNA occurred following the administration of GnRH, demonstrating that GnRH, and to a lesser degree E(2), negatively regulate Cres mRNA in gonadotropes. Examination of CRES protein by immunohistochemistry showed that levels were profoundly reduced following castration, while DHT and in part T, but not E(2), restored CRES levels. Castrated mice treated with Antide showed little effect. However, castrated mice treated with Antide + DHT showed a dramatic recovery of CRES, suggesting that androgens act directly at the level of the gonadotrope to regulate CRES protein. Together, our studies suggest that Cres mRNA and protein are low at peak gonadotrope secretory activity, possibly as a means to allow proprotein processing events to occur that are integral to gonadotrope function.
H G Sutton-Walsh; Sandra Whelly; Gail A Cornwall
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2006-07-12
Journal Detail:
Title:  Journal of andrology     Volume:  27     ISSN:  0196-3635     ISO Abbreviation:  J. Androl.     Publication Date:    2006 Nov-Dec
Date Detail:
Created Date:  2006-11-02     Completed Date:  2006-12-18     Revised Date:  2007-12-03    
Medline Journal Info:
Nlm Unique ID:  8106453     Medline TA:  J Androl     Country:  United States    
Other Details:
Languages:  eng     Pagination:  802-15     Citation Subset:  IM    
Department of Cell Biology and Biochemistry, Texas Tech University Health Sciences Center, Lubbock, TX 79430, USA.
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MeSH Terms
Androgens / physiology*
Cystatins / genetics*
Dihydrotestosterone / pharmacology
Estradiol / pharmacology
Gonadotrophs / drug effects,  physiology*
Gonadotropin-Releasing Hormone / physiology*
Luteinizing Hormone, beta Subunit / physiology
Mice, Inbred ICR
Oligopeptides / pharmacology
Organ Culture Techniques
RNA, Messenger / metabolism*
Substance Withdrawal Syndrome
Grant Support
Reg. No./Substance:
0/Androgens; 0/Cystatins; 0/Luteinizing Hormone, beta Subunit; 0/Oligopeptides; 0/RNA, Messenger; 112568-12-4/iturelix; 149291-61-2/Cst8 protein, mouse; 33515-09-2/Gonadotropin-Releasing Hormone; 50-28-2/Estradiol; 521-18-6/Dihydrotestosterone

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