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Review: Endocrine regulation of placental phenotype.

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Fowden, AL 
Forhead, AJ 
Sferruzzi-Perri, AN 
Burton, GJ 
Vaughan, OR 


Hormones have an important role in regulating fetal development. They act as environmental signals and integrate tissue growth and differentiation with relation to nutrient availability. While hormones control the developmental fate of resources available to the fetus, the actual supply of nutrients and oxygen to the fetus depends on the placenta. However, much less is known about the role of hormones in regulating placental development, even though the placenta has a wide range of hormone receptors and produces hormones itself from early in gestation. The placenta is, therefore, exposed to hormones by autocrine, paracrine and endocrine mechanisms throughout its lifespan. It is known to adapt its phenotype in response to environmental cues and fetal demand signals, particularly when there is a disparity between the fetal genetic drive for growth and the nutrient supply. These adaptive responses help to maintain fetal growth during adverse conditions and are likely to depend, at least in part, on the hormonal milieu. This review examines the endocrine regulation of placental phenotype with particular emphasis on the glucocorticoid hormones. It focuses on the availability of placental hormone receptors and on the effects of hormones on the morphology, transport capacity and endocrine function of the placenta.


This is the accepted manuscript for a paper published in Placenta Volume 36, Supplement 1, April 2015, Pages S50–S59, doi: 10.1016/j.placenta.2014.11.018


Hormones, Placental phenotype, Transport, Animals, Female, Fetal Development, Hormones, Humans, Maternal-Fetal Exchange, Phenotype, Placenta, Placental Hormones, Placentation, Pregnancy, Receptors, Cytoplasmic and Nuclear

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W.B. Saunders Ltd
Biotechnology and Biological Sciences Research Council (BB/I011773/1)
Wellcome Trust (084804/Z/08/Z)
We would like to thank the many members of the Department of Physiology, Development and Neuroscience who have contributed to discussions and helped with our own studies cited here. We are also grateful for financial support from the BBSRC (BB/I011773/1), Horserace Betting Levy Board (VET/PRJ/726 and 736), the Wellcome Trust 084804/2/08/Z and the Centre for Trophoblast Research at the University of Cambridge.