Prenatal programing: At the intersection of maternal stress and immune activation

We have found similar sex-specific effects of prenatal stress on the male placenta in mice

Christopher L. Howerton; Tracy L. Bale


Scholarcy highlights

  • Exposure to prenatal insults such as maternal stress and pathogenic infections has been associated with an increased risk for neurodevelopmental disorders
  • Compared to non-stressed controls, early prenatal stress produced male specific increases in placental gene expression of peroxisome proliferator-activated receptor α, insulin like growth factor binding protein 1, glucose transporter 4, and hypoxia-inducible factor 3α, all genes known to be critically important in regulating fetal growth and development
  • The sex-specific contribution of the placenta to fetal programing may be resultant from differential expression of sex-linked traits, such as NEMO, as opposed to the traditionally held view of the influences of gonadal hormones. Both maternal stress and immune activation serve as potentiating factors for alterations in offspring programing and increasing disease risk
  • Perhaps even more intriguing are the seemingly temporal- and sex-specific effects of these fetal antecedents. Careful consideration of these sensitive periods of increased vulnerability that are dependent on fetal sex will likely elucidate important mechanisms by which the maternal environment invokes long-term outcomes
  • It is clear that the endocrine placenta is a key target tissue in need of further analyses for its important roles in fetal development including: sexspecificity of the placenta, its dynamic changes in early development, and its role in endocrine signaling for factors critical in determining somatic growth and programing
  • Strategies to investigate the placenta in these programing events should focus on common factors of both the stress and immune pathways, as their activation during pregnancy promote similar offspring phenotypes

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