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Molecular Human Reproduction, Vol. 7, No. 9, 875-879, September 2001
© 2001 European Society of Human Reproduction and Embryology


Implantation and pregnancy

Interactions between progesterone receptor isoforms in myometrial cells in human labour

Doris Pieber1, Victoria C. Allport2, Frank Hills2, Mark Johnson3 and Phillip R. Bennett2,4

1 Department of Obstetrics and Gynaecology, Karl-Franzens University Graz, Austria, 2 Imperial College School of Medicine Parturition Research Group, Institute of Reproductive and Developmental Biology, Hammersmith Hospital, Du Cane Road, London W12 and 3 Department of Maternal & Fetal Medicine, Imperial College School of Medicine, Chelsea and Westminster Hospital, London, UK

Abstract

Progesterone acts to maintain uterine quiescence during pregnancy. In contrast to many other species, no decrease in maternal serum levels of progesterone can be observed in humans before the onset of labour. Therefore, a `functional' progesterone withdrawal in association with labour has been proposed. In humans the progesterone receptor (PR) exists in two isoforms, PR-A and PR-B. While PR-B generally mediates the effects of progesterone upon gene transcription, the role of PR-A during pregnancy, and in parturition, is unknown. In this study, term myometrium cells cultured before the onset of labour were transiently transfected with expression vectors for either PR-A or PR-B. Only those cells expressing PR-B significantly increased expression of a progesterone-sensitive reporter when stimulated with progesterone. Co-transfection of both isoforms of PR demonstrated that PR-A is a dominant repressor of transactivation in these cells. Western blot analysis showed that PR-A is present in human myometrium samples taken only after, but not before, the onset of labour. These data suggest that increased expression of PR-A in human myometrium may contribute to `functional' progesterone withdrawal and the initiation of human labour.

labour/myometrium/parturition/progesterone receptor

Notes

4 To whom correspondence should be addressed at: Division of Paediatrics, Obstetrics and Gynaecology, Institute of Obstetrics and Gynaecology, Imperial College School of Medicine, Queen Charlotte's and Chelsea Hospital, Ducane Road London W12 0HS, UK. E-mail: pbennett{at}ic.ac.uk


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