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Effects of dexamethasone and dibutyryl cAMP on stanniocalcin-1 mRNA expression in rat primary Sertoli and Leydig cells.

Authors: Li, L  Wong, CK 
Citation: Li L and Wong CK, Mol Cell Endocrinol. 2008 Feb 13;283(1-2):96-103. Epub 2007 Dec 3.
Pubmed: (View Article at PubMed) PMID:18187254
DOI: Full-text: DOI:10.1016/j.mce.2007.11.028

In this study, STC1 expression levels were determined at various postnatal developmental stages in rat ovaries and testes. The expression pattern of STC1 was found to be sexually dimorphic. In addition we examined the effect of exogenous glucocorticoids, dexamethasone (DEX), testosterone, follicle stimulating hormone (FSH) and dibutyryl cAMP (dbcAMP) on STC1 expression in rat primary Sertoli cell cultures. Our results showed that DEX (via glucocorticoids receptor) stimulated while dbcAMP inhibited STC1 expression in the Sertoli cells. Moreover testosterone and FSH treatment had no significant effect on STC1 expression in the cells. The inhibitory effect of dbcAMP to STC1 expression was consistently demonstrated in rat primary Leydig cell cultures. In human chorinoic gonadotropin (hCG) or dbcAMP treated Leydig cells, a significant reduction of STC1 expression was accompanied with an induction of testosterone secretion. The actions of hCG/dbcAMP were mediated by PKA, as the effect can be rescued by a co-treatment with H89. Using the Sertoli cell model, the modulation of STC1 expression by DEX or dbcAMP was found to be regulated at the transcriptional level as actinomycin D treatment significantly reduced the respective effect. In addition, both DEX and dbcAMP mediated effects were found to be abolished by cycloheximide co-treatment. These indicated that the regulation in the both treatments were indirect and may require prior protein synthesis. We suggested that the de novo synthesis of other protein(s) and mRNA may be involved in the regulation of the steady-state levels of STC1 mRNA in the treatments. Taken together, this study provides the first evidence of the regulation of STC1 expression in the male reproductive system.


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CRRD Object Information
CRRD ID: 2324697
Created: 2010-05-12
Species: All species
Last Modified: 2010-05-12
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.