Associations between maternal level of education and occupational status with placental glucocorticoid regeneration and sensitivity

Clin Endocrinol (Oxf). 2014 Aug;81(2):175-82. doi: 10.1111/cen.12412. Epub 2014 Feb 13.

Abstract

Objectives: Low socio-economic status (SES) is associated with increased disease risk in the involved and the next generation. The effects of low maternal SES on the offspring may be initiated prenatally. We hypothesized that fetoplacental glucocorticoid exposure might mediate the links. We examined associations between maternal level of education and occupational status (used as indices of SES) and placental expression of genes involved in glucocorticoid exposure and transfer between the mother and foetus.

Design and patients: Placental biopsies were obtained from 67 healthy women (age 32.2 ± 5.3 years) with singleton, term pregnancies without obstetric complications who participated in a prospective Prediction and Prevention of Preeclampsia (PREDO) study.

Measures: Level of education was self-reported, and occupational status was extracted from hospital records. Relative glucocorticoid receptor (GR; NR3C1), mineralocorticoid receptor (MR; NR3C2) and 11-beta-hydroxysteroid dehydrogenase type 1 (HSD11B1) and 2 (HSD11B2) mRNA levels were quantified by real-time PCR.

Results: Placental GR and HSD11B1 expression increased with decreasing maternal education (unadjusted P-values for linear trend = 0.04 and 0.02 and adjusted P-values = 0.06 and 0.09, respectively). Mothers with primary/secondary education had 52.9% (95% CI, 6.2-99.6, P = 0.03, adjusted P = 0.05) and 79.6% (95% CI, 6.5-153.6, P = 0.03, adjusted P = 0.09) higher GR and HSD11B1 mRNA levels compared with mothers with tertiary education. There were no other significant associations.

Conclusions: Lower maternal level of education is associated with increased placental GR and HSD11B1 gene expression. This combination may regenerate active glucocorticoids in placenta and increase placental sensitivity to glucocorticoids, potentially leading to greater placental and foetal glucocorticoid exposure.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 11-beta-Hydroxysteroid Dehydrogenase Type 1 / genetics
  • 11-beta-Hydroxysteroid Dehydrogenase Type 2 / genetics
  • Adult
  • Educational Status*
  • Employment*
  • Female
  • Humans
  • Male
  • Placenta / metabolism*
  • Pregnancy
  • Prospective Studies
  • RNA, Messenger
  • Real-Time Polymerase Chain Reaction
  • Receptors, Glucocorticoid / genetics
  • Receptors, Mineralocorticoid / genetics

Substances

  • NR3C1 protein, human
  • NR3C2 protein, human
  • RNA, Messenger
  • Receptors, Glucocorticoid
  • Receptors, Mineralocorticoid
  • 11-beta-Hydroxysteroid Dehydrogenase Type 1
  • 11-beta-Hydroxysteroid Dehydrogenase Type 2
  • HSD11B1 protein, human
  • HSD11B2 protein, human