Timing of Prenatal Exposure to Trauma and Altered Placental Expressions of HPA-Axis Genes and Genes Driving Neurodevelopment

Abstract

Prenatal maternal stress increases the risk for negative developmental outcomes in offspring, however the underlying biological mechanisms remain largely unexplored. In this study, alterations in placental gene expression associated with maternal stress were examined to elucidate potential underlying epi/genetic mechanisms. Expression levels of 40 selected genes involved in regulating fetal HPA-axis and neurodevelopment were profiled in placental tissues collected from a birth cohort established around the time of Superstorm Sandy. Objective prenatal traumatic stress was defined as whether mothers were exposed to Superstorm Sandy during pregnancy. Among the 275 mother-infant dyads, 181 dyads were delivered before Superstorm Sandy (i.e., Control), 66 dyads were exposed to Superstorm Sandy during the first trimester (i.e., Early Exposure) and 28 were exposed to Superstorm Sandy during the second or third trimester (i.e., Mid-Late Exposure). Across all trimesters, expression of HSD11B2, MAOA, ZNF507, and DYRK1A was downregulated among those exposed to Superstorm Sandy during pregnancy. Furthermore, trimester specific differences were also observed: exposure during early gestation was associated with downregulation of HSD11B1 and MAOB, and upregulation of CRHBP; exposure during mid-late gestation was associated with upregulation of SRD5A3. Our findings suggest that placental gene expression may be altered in response to traumatic stress exposure during pregnancy, and the susceptibility of these genes is dependent on the time of the exposure during pregnancy. Further studies can elucidate the biological mechanisms that underlie trimester-specific exposure by evaluating the differential impact on offspring neurodevelopment later in childhood.

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