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Endocrinology Vol. 143, No. 10 3984-3993
Copyright © 2002 by The Endocrine Society

ARTICLE

A Prostaglandin F2{alpha} Analog Induces Suppressors of Cytokine Signaling-3 Expression in the Corpus Luteum of the Pregnant Rat: A Potential New Mechanism in Luteolysis

J. D. Curlewis, S. P. Tam, P. Lau, D. H. L. Kusters, J. L. Barclay, S. T. Anderson and M. J. Waters

School of Biomedical Sciences, Department of Physiology and Pharmacology and Institute for Molecular Biosciences, University of Queensland, Queensland 4072, Australia

Address all correspondence and requests for reprints to: J. D. Curlewis, Ph.D., Department of Physiology and Pharmacology, University of Queensland, Queensland 4072, Australia. E-mail: .

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 F2{alpha} (PGF2{alpha}) might up-regulate SOCS proteins to inhibit PRL signaling. In d 19 pregnant rats, cloprostenol, a PGF2{alpha} 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 PGF2{alpha} may be an important element in the initiation of luteolysis via rapid suppression of luteotropic support from PL.




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