Maternal Stress and Placental RNA Expression and Methylation of the HSD11β2 Gene in Intrauterine Growth Restriction.

J. Miranda, C. Paules, S. Macias-Redondo, F. Crovetto, A. Basso, M. Gómez-Roig. E. Eixarch, O. Pozo, J. Schoorlemmer, F. Crispi, E. Gratacós (2017) OP01.08: Prenatal stress modifies RNA expression of HSD11β2 and the hypothalamic‐pituitary‐adrenocortical axis in fetal growth restriction.Ultrasound in Obstetrics and Gynecology 50(S1):50-50 Special Issue: Abstracts of the 27th World Congress on Ultrasound in Obstetrics and Gynecology, 16–19 September 2017, Vienna, Austria

To determine the role of maternal stress in sub‐optimal fetal growth and its relation with RNA expression and DNA methylation of the placental 11β‐HSD2.

Prospective cohort study in full‐term singleton gestations. Perceived Stress Scale (PSS) was assessed in pregnancies with suspected sub‐optimal fetal growth that subsequently delivered a small for gestational age (SGA) neonate (birthweight (BW)<10th centile; n=35) and in a control group with normally grown fetuses (n=26). SGA cases with a BW <3rd centile and/or abnormal Doppler were classified as fetal growth restriction (FGR). In addition, placental RNA expression and DNA methylation of HSD11β2 in 4 CpGs sites were also analysed.

The frequency of maternal stress (PSS>26) was significantly higher in cases than in controls [FGR: 33.3% and SGA: 36.3% vs. Controls: 7.7%; p=0.04]. Placental HSD11β2 RNA expression was significantly lower in cases than in controls [FGR: 0.45 (0.33 – 1.0) and SGA: 0.37 (0.21 – 0.68) vs. 1.1 (0.62 – 1.75); p=0.03 and 0.003, respectively] (Figure). There were no significant differences in the placental CpGs methylation of HSD11β2 sites across the groups. However, when groups were subdivided according to stress, SGA cases with maternal stress have a significantly different (%) of methylation in the median CpGs compared to controls.

Our findings indicate a significant association between maternal stress and suboptimal fetal growth, affecting RNA expression and DNA methylation of glucocorticoids‐related placenta genes in both, SGA and FGR fetuses.