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Am J Physiol Endocrinol Metab (August 6, 2002). doi:10.1152/ajpendo.00116.2002
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Articles in PresS, published online ahead of print August 6, 2002
Am J Physiol Endocrinol Metab, 10.1152/ajpendo.00116.2002
Submitted on March 14, 2002
Accepted on July 31, 2002

Messenger RNA for Progesterone Receptor Isoforms in the Late Gestation Rat Uterus

Xin Fang1, Susan Wong1, and Bryan F Mitchell1*

1 Department of Obstetrics and Gynecology, University of Alberta, Perinatal Research Centre, Edmonton, Alberta, Canada

* To whom correspondence should be addressed. E-mail: brymitch{at}ualberta.ca.

The progesterone receptor (PR) has three isoforms, PR-A, PR-B and PR-C, which have different physiologic effects. PR-A may inhibit PR-B-mediated transcription. Parturition requires withdrawal of progesterone (P4). This could occur through decreased P4 concentrations and/or a change in PR isoforms to diminish the effect of P4. We measured mRNA for PR isoforms in rat uterine tissues through late gestation and investigated the effects of antagonists to estrogen (tamoxifen) and P4 (RU486). Two specific probes were used for ribonuclease protection assays - one (PR-total) measured PR-A, PR-B and PR-C and the other recognized only PR-B. PR-total mRNA increased significantly through late gestation whereas PR-B was unchanged. The ratio of PR-total to PR-B peaked the day prior to parturition. Tamoxifen delayed parturition and inhibited the increase in PR-total without affecting PR-B mRNA. RU486 caused early parturition associated with increased PR-total mRNA with no change in PR-B. We conclude there are significant changes in PR isoforms in late gestation rat uterus. These changes may be regulated by estrogen and P4 and may influence the timing of parturition.




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