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Int. J. Mol. Sci. 2015, 16(11), 27482-27496; doi:10.3390/ijms161126034

Maternal Prenatal Mental Health and Placental 11β-HSD2 Gene Expression: Initial Findings from the Mercy Pregnancy and Emotional Wellbeing Study

1
School of Psychology, Deakin University, Melbourne 3125, Australia
2
Centre for Social and Early Emotional Development, Deakin University, Melbourne 3125, Australia
3
Cancer and Disease Epigenetics, Murdoch Childrens Research Institute and Department of Paediatrics, University of Melbourne, Parkville 3052, Australia
4
Mercy Perinatal Research Centre, Mercy Hospital for Women, Melbourne 3084, Australia
5
Obstetrics, Nutrition and Endocrinology Group, Department of Obstetrics and Gynaecology, University of Melbourne, Parkville 3052, Australia
6
Department of Perinatal Mental Health, Mercy Hospital for Women, Melbourne 3084, Australia
*
Author to whom correspondence should be addressed.
Academic Editor: Kenji Hashimoto
Received: 6 September 2015 / Revised: 1 November 2015 / Accepted: 3 November 2015 / Published: 17 November 2015
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Abstract

High intrauterine cortisol exposure can inhibit fetal growth and have programming effects for the child’s subsequent stress reactivity. Placental 11beta-hydroxysteroid dehydrogenase (11β-HSD2) limits the amount of maternal cortisol transferred to the fetus. However, the relationship between maternal psychopathology and 11β-HSD2 remains poorly defined. This study examined the effect of maternal depressive disorder, antidepressant use and symptoms of depression and anxiety in pregnancy on placental 11β-HSD2 gene (HSD11B2) expression. Drawing on data from the Mercy Pregnancy and Emotional Wellbeing Study, placental HSD11B2 expression was compared among 33 pregnant women, who were selected based on membership of three groups; depressed (untreated), taking antidepressants and controls. Furthermore, associations between placental HSD11B2 and scores on the State-Trait Anxiety Inventory (STAI) and Edinburgh Postnatal Depression Scale (EPDS) during 12–18 and 28–34 weeks gestation were examined. Findings revealed negative correlations between HSD11B2 and both the EPDS and STAI (r = −0.11 to −0.28), with associations being particularly prominent during late gestation. Depressed and antidepressant exposed groups also displayed markedly lower placental HSD11B2 expression levels than controls. These findings suggest that maternal depression and anxiety may impact on fetal programming by down-regulating HSD11B2, and antidepressant treatment alone is unlikely to protect against this effect. View Full-Text
Keywords: 11-beta hydroxysteroid dehydrogenase type 2; placenta 11β-HSD2; HSD11B2; prenatal depression; prenatal anxiety; cortisol; fetal programming 11-beta hydroxysteroid dehydrogenase type 2; placenta 11β-HSD2; HSD11B2; prenatal depression; prenatal anxiety; cortisol; fetal programming
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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MDPI and ACS Style

Seth, S.; Lewis, A.J.; Saffery, R.; Lappas, M.; Galbally, M. Maternal Prenatal Mental Health and Placental 11β-HSD2 Gene Expression: Initial Findings from the Mercy Pregnancy and Emotional Wellbeing Study. Int. J. Mol. Sci. 2015, 16, 27482-27496.

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