The significance of the placental genome and methylome in fetal and maternal health
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REVIEW
The significance of the placental genome and methylome in fetal and maternal health Giulia F. Del Gobbo1,2 · Chaini Konwar1,2 · Wendy P. Robinson1,2 Received: 19 January 2019 / Accepted: 29 August 2019 © Springer-Verlag GmbH Germany, part of Springer Nature 2019
Abstract The placenta is a crucial organ for supporting a healthy pregnancy, and defective development or function of the placenta is implicated in a number of complications of pregnancy that affect both maternal and fetal health, including maternal preeclampsia, fetal growth restriction, and spontaneous preterm birth. In this review, we highlight the role of the placental genome in mediating fetal and maternal health by discussing the impact of a variety of genetic alterations, from large whole-chromosome aneuploidies to single-nucleotide variants, on placental development and function. We also discuss the placental methylome in relation to its potential applications for refining diagnosis, predicting pathology, and identifying genetic variants with potential functional significance. We conclude that understanding the influence of the placental genome on common placental-mediated pathologies is critical to improving perinatal health outcomes.
Introduction The placenta is the key mediator of maternal and fetal health during pregnancy. It is a highly adaptive organ that responds to maternal and fetal signals, shows remarkable variability in size and shape, and can tolerate some degree of localized pathology while still able to support fetal growth to term. Nevertheless, abnormal development or function of the placenta underlies many complications of pregnancy including miscarriage, maternal preeclampsia (PE), fetal growth restriction (FGR), preterm birth (PTB), and fetal malformation (Burton and Jauniaux 2018; Morgan 2016). Chromosome imbalance, genetic variation, and epigenetic changes have been implicated and/or associated with these Giulia F. Del Gobbo and Chaini Konwar have contributed equally. * Wendy P. Robinson [email protected] Giulia F. Del Gobbo [email protected] Chaini Konwar [email protected] 1
BC Children’s Hospital Research Institute, 950 West 28th Ave, Vancouver, BC V5Z 4H4, Canada
Department of Medical Genetics, University of British Columbia, 4500 Oak Street, Vancouver, BC V6H 3N1, Canada
2
conditions, although our knowledge of normal and abnormal genomic variation in the placenta is still maturing. The placental genome is normally identical to that of the fetus, as both are developmentally derived from the conceptus. However, this can differ due to mosaicism (or more rarely, chimerism) discussed further below. The placenta also interfaces directly with the maternal decidua, which derives from a thickening and modification of the uterine wall during pregnancy and is shed along with the placenta at parturition. Within the decidua, there is an intermingling of placental-derived cells and maternal cells, as a subset of placental trophoblast cells migrate into the maternal tissue both to anchor the placenta into the ute
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