期刊
PSYCHOLOGICAL MEDICINE
卷 45, 期 10, 页码 2023-2030出版社
CAMBRIDGE UNIV PRESS
DOI: 10.1017/S003329171400316X
关键词
Depression; glucocorticoid receptors; mineralocorticoid receptors; placenta; pregnancy
资金
- Academy of Finland
- Signe and Ane Gyllenberg Foundation
- Emil Aaltonen Foundation, EVO
- Finnish Medical Foundation
- Jane and Aatos Erkko Foundation
- Novo Nordisk Foundation
- Paivikki and Sakari Sohlberg Foundation
- Sigrid Juselius Foundation
- University of Helsinki
- Sir Jules Thorn Charitable Trust
- Chief Scientist Office [CZG/2/478] Funding Source: researchfish
- Novo Nordisk Fonden [NNF12OC1016374] Funding Source: researchfish
Background. Maternal prenatal depression predicts post-partum depression and increases risk of prematurity and low birth weight. These effects may be mediated by altered placental function. We hypothesized that placental function would be influenced by the gestational week of experiencing depressive symptoms and aimed to examine associations between maternal depressive symptoms during pregnancy and placental expression of genes involved in glucocorticoid and serotonin transfer between mother and fetus. Method. We studied women participating in a prospective pregnancy cohort: the Prediction and Prevention of Preeclampsia (PREDO) Study, Helsinki, Finland. Maternal depressive symptoms were assessed at 2-week intervals throughout pregnancy in 56 healthy women with singleton, term pregnancies. Messenger ribonucleic acid (mRNA) levels of glucocorticoid (GR) and mineralocorticoid (MR) receptors and serotonin transporter (SLC6A4), 11 beta-hydroxysteroid dehydrogenase type 1 (HSD1) and 2 (HSD2) were quantified in placental biopsies. Results. In adjusted analyses women who reported higher depressive symptoms across the whole pregnancy had higher mRNA levels of GR [effect size 0.31 S.D. units, 95% confidence interval (CI) 0.01-0.60, p = 0.042] and MR (effect size 0.34 S.D. units, 95% CI 0.01-0.68, p = 0.047). These effects were significant for symptoms experienced in the third trimester of pregnancy for GR; findings for MR were also significant for symptoms experienced in the second trimester. GR and MR mRNA levels increased linearly by having the trimester-specific depressive symptoms scores 0, 1 or 2-3 times above the clinical cut-off for depression (p = 0.003, p = 0.049, respectively, and p = 0.004, p = 0.15 in adjusted analyses). Conclusions. Our findings offer potential gestational-age-specific mechanisms linking maternal depressive symptoms during pregnancy via placental biology. Future studies will test whether these also link with adverse offspring outcomes.
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