Maternal Chronic Stress Induced Placental Epigenetic Changes in Hydroxysteroid dehydrogenase 11-beta II Promoter Leading to Increased Risk of Preeclampsia

Abstract

Preeclampsia is a gestational condition characterized by hypertension that can result in severe consequences for both the mother and fetus. Affecting roughly 8% of pregnancies in the United States, preeclamptic mothers exhibit lower expression of the protein 11-beta-hydroxysteroid dehydrogenase II (11βHSD2) that functions to regulate placental glucocorticoid exposure. Impaired 11βHSD2 function results in high cortisol levels in the maternal plasma, and thus dangerous exposure of excessive cortisol to the fetus. The etiology behind the pathological behavior of preeclampsia is still unknown, however, several studies have supported the prediction that the decrease in 11βHSD2 expression may be due to epigenetic changes to the gene responsible for 11βHSD2 transcription, hydroxysteroid dehydrogenase 11-beta II (HSD11β2). Epigenetic changes to the genome are the result of environmental exposure, including exposure to chronic stress. In the case of preeclampsia, this capstone will explore the hypothesis of the potential effects of maternal exposure to chronic stress that causes epigenetic changes to the promoter region HSD11β2 in the placenta resulting in lower expression of 11βHSD2 and an increased risk of preeclampsia in the mother.