Document Detail


Hormonal regulation of suppressors of cytokine signaling (SOCS) messenger ribonucleic acid in the arcuate nucleus during late pregnancy.
MedLine Citation:
PMID:  18325991     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Prolactin stimulates tuberoinfundibular dopamine neurons in the arcuate nucleus of the hypothalamus, mediated by signal transducer and activator of transcription 5b (STAT5b). During late pregnancy, these neurons become unresponsive to prolactin, with a loss of prolactin-induced activation of STAT5b and decreased dopamine secretion. Suppressors of cytokine signaling (SOCS) proteins inhibit STAT-mediated signaling, and SOCS mRNAs are specifically elevated in the arcuate nucleus during late pregnancy. We hypothesized that changes in circulating ovarian steroids during late pregnancy might induce expression of SOCS mRNAs, thus disrupting STAT5b-mediated prolactin signaling. Rats were ovariectomized on d 18 of pregnancy and treated with ovarian steroids to simulate an advanced, normal, or delayed decline in progesterone. Early progesterone withdrawal caused an early increase in prolactin secretion, and increased SOCS-1 and -3 and cytokine-inducible SH2-containing protein (CIS) mRNA levels in the arcuate nucleus. Prolonged progesterone treatment prevented these changes. To determine whether ovarian steroids directly alter SOCS mRNA levels, estrogen- and/or progesterone-treated ovariectomized nonpregnant rats were acutely injected with prolactin (300 microg sc) or vehicle. SOCS-1 and -3 and CIS mRNA levels in the arcuate nucleus were significantly increased by estrogen or prolactin, whereas progesterone treatment reversed the effect of estrogen. Results demonstrate that estrogen and prolactin can independently induce SOCS mRNA in the arcuate nucleus and that this effect is negatively regulated by progesterone. This is consistent with the hypothesis that declining progesterone and high levels of estrogen during late pregnancy induce SOCS in the tuberoinfundibular dopamine neurons, thus contributing to their insensitivity to prolactin at this time.
Authors:
Frederik J Steyn; Greg M Anderson; David R Grattan
Publication Detail:
Type:  Journal Article     Date:  2008-03-06
Journal Detail:
Title:  Endocrinology     Volume:  149     ISSN:  0013-7227     ISO Abbreviation:  Endocrinology     Publication Date:  2008 Jun 
Date Detail:
Created Date:  2008-05-21     Completed Date:  2008-08-08     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0375040     Medline TA:  Endocrinology     Country:  United States    
Other Details:
Languages:  eng     Pagination:  3206-14     Citation Subset:  AIM; IM    
Affiliation:
Centre for Neuroendocrinology and Department of Anatomy and Structural Biology, University of Otago School of Medical Sciences, PO Box 913, Dunedin 9054, New Zealand.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Arcuate Nucleus / physiology*
Estrogens / pharmacology
Female
Gene Expression Regulation
Pregnancy
Pregnancy, Animal / physiology*
Progesterone / pharmacology
Prolactin / drug effects,  physiology
RNA, Messenger / genetics
Rats
Rats, Sprague-Dawley
Suppressor of Cytokine Signaling Proteins / genetics*
Chemical
Reg. No./Substance:
0/Estrogens; 0/RNA, Messenger; 0/Socs1 protein, mouse; 0/Socs3 protein, mouse; 0/Suppressor of Cytokine Signaling Proteins; 57-83-0/Progesterone; 9002-62-4/Prolactin

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Active intestinal calcium transport in the absence of transient receptor potential vanilloid type 6 ...
Next Document:  Infertility in females with cystic fibrosis is multifactorial: evidence from mouse models.