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Epigenetics and the placenta

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TLDR
Epigenetic regulation of the placenta evolves during preimplantation development and further gestation and appears to be involved in the pathogenesis of pre-eclampsia and GTD.
Abstract
results: Epigenetic regulation of the placenta evolves during preimplantation development and further gestation. Epigenetic marks, like DNA methylation, histone modifications and non-coding RNAs, affect gene expression patterns. These expression patterns, including the important parent-of-origin-dependent gene expression resulting from genomic imprinting, play a pivotal role in proper fetal and placental development. Disturbed placental epigenetics has been demonstrated in cases of intrauterine growth retardation and small for gestational age, and also appears to be involved in the pathogenesis of pre-eclampsia and GTD. Several environmental effects have been investigated so far, e.g. ethanol, oxygen tension as well as the effect of several aspects of assisted reproduction technologies on placental epigenetics. conclusions: Studies in both animals and humans have made it increasingly clear that proper epigenetic regulation of both imprinted and non-imprinted genes is important in placental development. Its disturbance, which can be caused by various environmental factors, can lead to abnormal placental development and function with possible consequences for maternal morbidity, fetal development and disease susceptibility in later life.

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Why do singletons conceived after assisted reproduction technology have adverse perinatal outcome? Systematic review and meta-analysis

TL;DR: Subfertility is a major risk factor for adverse perinatal outcome in ART singletons, however, even in the same mother an ART singleton has a poorer outcome than the non-ART sibling; hence, factors related to the hormone stimulation and/or IVF methods per se also may play a part.
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Linking prenatal maternal adversity to developmental outcomes in infants: The role of epigenetic pathways

TL;DR: Evidence illustrating the association between maternal prenatal distress and both fetal and infant developmental trajectories and the potential role of epigenetic mechanisms in mediating these effects are discussed.
Journal ArticleDOI

Sex-Specific Placental Responses in Fetal Development

TL;DR: Evidence that various species, including humans, exhibit normal sex-dependent structural and functional placental differences will be examined followed by how in utero environmental changes (nutritional state, stress, and exposure to environmental chemicals) might interact with fetal sex to affect this organ.
Journal ArticleDOI

Environmental epigenetics: prospects for studying epigenetic mediation of exposure–response relationships

TL;DR: Some of the challenges in studying epigenetic mediation of pathogenesis are discussed and some unique opportunities for exploring these phenomena are described.
References
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Journal ArticleDOI

Tumor suppressor and growth regulatory genes are overexpressed in severe early-onset preeclampsia - an array study on case-specific human preeclamptic placental tissue

TL;DR: DNA array technique was used to compare placental gene expression profile in severe early‐onset preeclampsia from 25 to 27 gestational weeks with strictly non‐affected placental samples from similar gestational Weeks.
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Expression profile and transcription factor binding site exploration of imprinted genes in human and mouse.

TL;DR: A computational analysis of microarray expression data of imprinted genes in human and mouse placentae and in a variety of adult tissues reveals correlation of tissue-specific expression patterns and the presence of distinct TFBS signatures in the upstream region of human imprinting genes.
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Epigenetics and Imprinting of the Trophoblast – A Workshop Report

TL;DR: A series of short talks were presented providing an overview of the evolution, function and mechanisms of imprinting in mammals with particular reference to the placenta, and epigenetic control of trophoblast development and function were considered.
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Evolutionary genetic models of the ovarian time bomb hypothesis for the evolution of genomic imprinting.

TL;DR: This study examines the "ovarian time bomb" hypothesis, which proposes that imprinting arose through selection for reduced risk of ovarian trophoblastic disease in females and presents three evolutionary genetic models that incorporate both this selection pressure and the effect of deleterious mutations to elucidate the conditions under which imprinting could evolve.
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Differential downregulation of αT-catenin expression in placenta: trophoblast cell type-dependent imprinting of the CTNNA3 gene

TL;DR: It is demonstrated that the CTNNA3 gene is subject to imprinting with preferential expression of the maternal allele in first trimester placental tissues, suggesting that gene dosage compensation of CTNna3 and p57KIP2 in the placenta shares a conserved regulatory mechanism that correlates with an early step in trophoblast determination, i.e. differentiation into villus or extravillus trophOBlast.
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