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Epigenetic regulation of the placental HSD11B2 barrier and its role as a critical regulator of fetal development

Togher, K. L. and O'Keeffe, M. M. and Khashan, A. S. and Gutierrez, Humberto and Kenny, L. C. and O'Keeffe, G. W. (2014) Epigenetic regulation of the placental HSD11B2 barrier and its role as a critical regulator of fetal development. Epigenetics, 9 (6). pp. 816-822. ISSN 1559-2294

Full content URL: https://www.landesbioscience.com/journals/epigenet...

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Item Type:Article
Item Status:Live Archive

Abstract

"Fetal programming" is a term used to describe how early-life experience influences fetal development and later disease risk. In humans, prenatal stress-induced fetal programming is associated with increased risk of preterm birth, and a heightened risk of metabolic and neurological diseases later in life. A critical determinant of this is the regulation of fetal exposure to glucocorticoids by the placenta. Glucocorticoids are the mediators through which maternal stress influences fetal development. Excessive fetal glucocorticoid exposure during pregnancy results in low birth weight and abnormalities in a number of tissues. The amount of fetal exposure to maternal glucocorticoids depends on the expression of HSD11B2, an enzyme predominantly produced by the syncytiotrophoblast in the placenta. This protects the fetus by converting active glucocorticoids into inactive forms. In this review we examine recent findings regarding placental HSD11B2 that suggest that its epigenetic regulation may mechanistically link maternal stress and long-term health consequences in affected offspring. © 2014 Landes Bioscience.

Keywords:11beta hydroxysteroid dehydrogenase 2, glucocorticoid, interleukin 1beta, messenger RNA, tumor necrosis factor alpha, adrenal cortex atrophy, amniocentesis, CpG island, epigenetics, female, fetus development, gene, gene expression, gene expression regulation, HSD11B2 gene, human, intrauterine growth retardation, low birth weight, metabolic disorder, neurologic disease, nonhuman, pregnancy outcome, premature labor, prenatal exposure, prenatal stress, protein microarray, rat, review, NotOAChecked
Subjects:C Biological Sciences > C140 Developmental/Reproductive Biology
C Biological Sciences > C431 Medical Genetics
Divisions:College of Science > School of Life Sciences
ID Code:14389
Deposited On:11 Jul 2014 08:35

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