Maternal prenatal anxiety and downregulation of placental 11β-HSD2.
|Title||Maternal prenatal anxiety and downregulation of placental 11β-HSD2.|
|Publication Type||Journal Article|
|Year of Publication||2012|
|Authors||O'Donnell K, Jensen ABugge, Freeman L, Khalife N, O'Connor TG, Glover V|
|Date Published||2012 Jun|
|Keywords||11-beta-Hydroxysteroid Dehydrogenase Type 2, Adult, Affect, Anxiety, Cesarean Section, Depression, Down-Regulation, Female, Gene Expression Regulation, Enzymologic, Humans, Male, Placenta, Pregnancy, Real-Time Polymerase Chain Reaction, RNA, Socioeconomic Factors, Surveys and Questionnaires|
BACKGROUND: Raised maternal anxiety during pregnancy is associated with increased risk of adverse neurodevelopmental outcomes for her child. The mechanisms underlying this are not known but animal studies suggest prenatal stress may alter the function of the placenta. Here we determined whether maternal prenatal anxiety was associated with a downregulation of placental 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2), the enzyme which metabolises cortisol.METHODS: We recruited mothers the day before delivery by elective caesarean, and gave them the Spielberger Trait and State anxiety and Edinburgh Depression self-rating scales. Placentae were collected and aliquots stored for later analysis.RESULTS: Prenatal Trait anxiety was negatively correlated with placental 11β-HSD2 mRNA expression (r=-0.40, p<0.01, n=56). Results were similar with male and female fetuses (r=-0.39, p=0.04, n=28; r=-0.40, p=0.03, n=28) respectively. Results were also significant with State anxiety (r=-0.27, p=0.05, n=56) but somewhat weaker for depression (r=-0.20, p=0.13, n=56). Preliminary analyses on a subset of cases (n=25) suggested parallel results for enzyme activity.CONCLUSIONS: These findings provide evidence for an association between prenatal maternal mood and downregulation of placental 11β-HSD2. Results are consistent with raised maternal anxiety being associated with increased fetal exposure to maternal cortisol, and support the hypothesis that this may be one mechanism underlying fetal programming by prenatal stress.
|Grant List||MC_G0802845 / / Medical Research Council / United Kingdom |
R01 MH073842 / MH / NIMH NIH HHS / United States
/ / Medical Research Council / United Kingdom