Document Detail


Maximal expression of suppressors of cytokine signaling in the rat ovary occurs in late pregnancy.
MedLine Citation:
PMID:  19502454     Owner:  NLM     Status:  In-Process    
Abstract/OtherAbstract:
Maintenance of the rodent corpus luteum (CL) during pregnancy requires prolactin receptor (PRLR) signal transduction via STAT5. At the end of pregnancy, prostaglandin F2alpha (PGF(2alpha)) induces luteal regression through many mechanisms, including downregulation of PRLR signaling. We have previously shown that a PGF(2alpha) analog upregulates suppressors of cytokine signaling (SOCS) proteins in the CL of day 19 pregnant rats leading to reduced STAT5 signaling. Here, we examined endogenous SOCS expression and STAT5 signaling in the rat ovary during normal pregnancy and luteolysis. The mRNA expression of Socs1, Socs2, and Socs3 and related cytokine-inducible SH2-containing protein (Cish) was low in early pregnancy (day 7), but significantly increased at mid-pregnancy (days 10 and 13) associated with increased endogenous tyrosine phosphorylation (TyrP) of STAT5. In support of the notion that these changes are due to increasing placental lactogen levels at this time, we found that treatment with exogenous PRL on day 7 increased TyrP of STAT5 and induced SOCS mRNA expression, except Socs3. After mid-pregnancy, further significant increases in Socs3 and Cish mRNA expression were observed. Such changes in mRNA expression correlated with protein levels, with protein levels of both SOCS3 and CISH being maximal in late pregnancy (days 19-21). In addition, a significant reduction in TyrP of STAT5 was first observed on day 20, with a further substantial decrease on day 21. Therefore, these results are consistent with the hypothesis that increased SOCS expression in the rat ovary during late pregnancy reduces STAT5 signaling, which may be important in PGF(2alpha)-induced luteolysis.
Authors:
Stephen T Anderson; Naajia N M Isa; Johanna L Barclay; Michael J Waters; Jon D Curlewis
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-06-05
Journal Detail:
Title:  Reproduction (Cambridge, England)     Volume:  138     ISSN:  1741-7899     ISO Abbreviation:  Reproduction     Publication Date:  2009 Sep 
Date Detail:
Created Date:  2009-08-25     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100966036     Medline TA:  Reproduction     Country:  England    
Other Details:
Languages:  eng     Pagination:  537-44     Citation Subset:  IM    
Affiliation:
School of Biomedical Sciences, School of Animal Studies Institute for Molecular Biosciences, The University of Queensland, St Lucia, Queensland 4072, Australia. stephen.anderson@uq.edu.au
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