Research ArticlePhysiology

RelB/p52-mediated NF-κB signaling alters histone acetylation to increase the abundance of corticotropin-releasing hormone in human placenta

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Science Signaling  25 Aug 2015:
Vol. 8, Issue 391, pp. ra85
DOI: 10.1126/scisignal.aaa9806

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Epigenetics in stress and labor

Pregnancy and labor are regulated by fluctuating hormone levels. Glucocorticoids stimulate production of the stress-responsive corticotropin-releasing hormone (CRH) in the placenta as the fetus nears full term. Using cultured primary trophoblasts isolated from midtrimester and full-term placenta, Di Stefano et al. found that glucocorticoids promote the expression of CRH by stimulating dynamic histone acetylation mediated by the binding of a complex containing the transcription factor nuclear factor κB (NF-κB), a histone lysine acetyltransferase, and a histone deacetylase to the CRH promoter. The findings reveal an epigenetic mechanism regulating the duration of pregnancy.