A prostaglandin F2a Analog induces suppressors of the cytokine signalling-3 expression n the corpus luteum of the pregnant rat: A potential new mechanism in luteolysis

Curlewis, J. D., Sau-Ping, T., Lau, W. F. P., Kusters, D. H. L., Barclay, J, Anderson, S. T. and Waters, M. J. (2002) A prostaglandin F2a Analog induces suppressors of the cytokine signalling-3 expression n the corpus luteum of the pregnant rat: A potential new mechanism in luteolysis. Endocrinology, 143 10: 3984-3993.


Author Curlewis, J. D.
Sau-Ping, T.
Lau, W. F. P.
Kusters, D. H. L.
Barclay, J
Anderson, S. T.
Waters, M. J.
Title A prostaglandin F2a Analog induces suppressors of the cytokine signalling-3 expression n the corpus luteum of the pregnant rat: A potential new mechanism in luteolysis
Journal name Endocrinology   Check publisher's open access policy
Publication date 2002
Sub-type Article
DOI 10.1210/en.2002-220344
Volume number 143
Issue number 10
ISSN 0013-7227
Start page 3984
End page 3993
Total pages 10
Editor Kenneth Korach
Place of publication USA
Publisher The Endocrine Society
Collection year 2002
Language eng
Subject C1
320602 Cell Physiology
780105 Biological sciences
Abstract PRL and placental lactogen (PL) play key roles in maintaining the rodent corpus luteum through pregnancy. Suppressors of cytokine signaling (SOCS) have been shown to decrease cell sensitivity to cytokines, including PRL, and so here we have addressed the issue of whether luteolysis induced by prostaglandin F-2alpha (PGF(2alpha)) might up-regulate SOCS proteins to inhibit PRL signaling. In d 19 pregnant rats, cloprostenol, a PGF(2alpha) analog, rapidly induced transcripts for SOCS-3 and, to a lesser extent, SOCS-1. We also found increased SOCS-3 protein in the ovary by immunoblot and in the corpus luteum by immunohistochemistry. Increased SOCS-3 expression was preceded by an increase in STAT3 tyrosine phosphorylation 10 min after cloprostenol injection and was maintained for 4 h, as determined by gel shift and immunohistochemistry. Induction of SOCS-3 was accompanied by a sharp decrease in active STAT5, as determined by gel-shift assay and by loss of nuclear localized STAT5. Four hours after cloprostenol administration, the corpus luteum was refractory to stimulation of STAT5 by PRL administration, and this was not due to down-regulation of PRL receptor. Therefore, induction of SOCS-3 by PGF(2alpha) may be an important element in the initiation of luteolysis via rapid suppression of luteotropic support from PL.
Keyword Endocrinology & Metabolism
Messenger-ribonucleic-acid
Protein-coupled Receptors
High-density Lipoproteins
Prolactin Receptor
Gene-expression
Tyrosine Kinase
20-alpha-hydroxysteroid Dehydrogenase
Luteinizing-hormone
Jak/stat Pathway
Angiotensin-ii
Q-Index Code C1

Document type: Journal Article
Sub-type: Article
Collections: Excellence in Research Australia (ERA) - Collection
School of Biomedical Sciences Publications
 
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