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Endocrine Abstracts (2012) 29 S17.2

ICEECE2012 Symposia Hormonal control of pregnancy (3 abstracts)

What controls labour in humans?

R. Smith


John Hunter Hospital, Newcastle, New South Wales, Australia.


In most mammals the onset of labour is regulated by an abrupt fall in circulating progesterone concentrations or a rise in circulating oestrogens. In humans, however, no dramatic change is observed in circulating steroid concentrations prior to labour and the mechanisms regulating the onset of labour have remained obscure. In a series of studies we have shown that placental production of the peptide hormone CRH increases exponentially across gestation peaking at the time of labour. We have also shown that CRH can exert direct actions on the fetal adrenal to stimulate production of DHEA which is 16 hydroxylated in the fetal adrenal and then converted to estriol in the placenta. The exponential increase in CRH drives a rise in estriol production in late gestation leading to a progressive increase in the ratio of estriol to estradiol (which is derived largely from maternal precursors). The increase in ratio of estriol to estradiol leads to activation of estrogen responsive genes and the onset of labour. Recently it has become apparent that the increase in placental CRH production is the result of expression of endogenous retroviruses in the placenta. The retrovirus gene product Syncytin promotes cytotrophoblast fusion and CRH expression. Data also indicates that CRH can directly increase placental estrogen synthesis and inhibit progesterone synthesis. Thus CRH plays a central role in modifying the placental endocrine environment to promote labour. It is not yet clear how this links to the expression of the myometrial proteins that regulate myometrial contraction including the progesterone receptors, connexin 43 and the changes in ion channels that regulate myometrial excitability. It may be that prostaglandins are stimulated by CRH and then regulate progesterone isoforms expression by changing the epigenetic marks on the promoters of the progesterone receptor promoters.

Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.

Funding: This research did not receive any specific grant from any funding agency in the public, commercial or not-for-profit sector.

Volume 29

15th International & 14th European Congress of Endocrinology

European Society of Endocrinology 

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