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

Sunaina Seth, Andrew James Lewis, Richard Saffery, Martha Lappas, Megan Galbally

Research output: Contribution to journalArticlepeer-review

58 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)27482-96
Number of pages15
JournalInternational Journal of Molecular Sciences
Volume16
Issue number11
DOIs
Publication statusPublished - 17 Nov 2015
Externally publishedYes

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