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Mol Cell Endocrinol. 2017 May 15;447:79-86. doi: 10.1016/j.mce.2017.02.034. Epub 2017 Feb 22.

11β-hydroxysteroid dehydrogenase type 1 and pregnancy: Role in the timing of labour onset and in myometrial contraction.

Author information

1
Department of Molecular and Developmental Medicine, University of Siena, Siena, Italy. Electronic address: francesco.damiani@yahoo.com.
2
Tommy's Centre for Maternal and Fetal Health at the Medical Research Council Centre for Reproductive Health, University of Edinburgh, Queen's Medical Research Institute, Edinburgh, United Kingdom.
3
Department of Molecular and Developmental Medicine, University of Siena, Siena, Italy.

Abstract

Glucocorticoids play a primary role in the maturation of fetal organs and may contribute to the onset of labour. Glucocorticoid activity depends on the 11β-hydroxysteroid dehydrogenase family (11β-HSDs), catalysing the interconversion between "active" cortisol into inactive cortisone. No definitive study exists on 11β-HSD expression profile in human decidua and myometrium during pregnancy. We investigated the implications of 11β-HSD1 in the regulation of uterine activity in pregnancy, examining its role on contraction of a myocyte cell line and murine 11β-hsd1 levels in utero. Murine 11β-hsd1 mRNA and protein levels in utero progressively increased until the last day of gestation and significantly decreased at the onset of labour (P < 0.0001) (n = 3 to 5 in the various gestational days analysed). Experiments on human myometrial samples confirm the significant fall in 11β-hsd1 mRNA levels at labour, compared to end pregnancy samples (n = 5 to 8). In vitro experiments showed that human myometrial contraction is inhibited by using a non-selective inhibitor of 11β-HSD1. The present study shows the temporal localisation of 11β-HSD1 in uterus, highlighting its importance in the timing of gestation and suggesting its contribution in the myometrium contraction.

KEYWORDS:

11beta-HSD; Cortisol; Labour; Myometrium; Pregnancy

PMID:
28237720
DOI:
10.1016/j.mce.2017.02.034
[Indexed for MEDLINE]

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