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Pregnancy

Fetal signalling initiates parturition

Nature Reviews Endocrinology volume 11, page 505 (2015)Cite this article

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Parturition is thought to be initiated by an increased inflammatory response and expression of contractile proteins in the uterine tissues, but the underlying mechanism is unclear. Pulmonary surfactant-associated protein-A (SP-A), which is secreted from the fetal lungs is thought to inititate this process. Now, new data indicate that nuclear receptor coactivators 1 and 2 (also known as steroid receptor coactivators; SRC-1 and SRC-2), regulates transcription of SP-A and consequently induction of labour.

In mice with heterozygous mutations in both SRC-1 and SRC-2 (SRC-1/-2 dhet), which avoids the lethality seen in double knockout mice, parturition was delayed by ∼38 h compared with wild-type mice. Interestingly, this delay was also seen in wild-type mice with SRC-1/-2 deficient embryos, which suggests that the signal to initiate labour is derived from the fetus.

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References

  1. Gao, L. et al. Steroid receptor coactivators 1 and 2 mediate fetal-to-maternal signaling that initiates parturition. J. Clin. Invest. 10.1172/JCI78544

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  1. Tim Geach
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Geach, T. Fetal signalling initiates parturition. Nat Rev Endocrinol 11, 505 (2015). https://doi.org/10.1038/nrendo.2015.115

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