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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.
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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

Current understandings of the molecular genetics of gestational trophoblastic diseases.

TL;DR: expression of telomerase activity, altered expression of cell--cell adhesion molecules and abnormal expression of matrix metalloproteinases have also been reported in GTD, which represent disruption of the delicate balance and regulation of cellular processes including proliferation, differentiation, apoptosis and invasion.
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The Regulation and Biological Significance of Genomic Imprinting in Mammals

TL;DR: The relationship between parental imprinting and the expression profiles of Pegs and Megs is outlined, a novel view of the regulation of genomic imprinting is discussed and hypotheses on the essential nature and close relationship between genomic imprinted and the acquisition of placental tissues during mammalian evolution are proposed.
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Epigenetic landscape required for placental development.

TL;DR: Investigations of the epigenetic regulation of transcriptional states will provide valuable insights into the dynamic chromatin environment that is specific to extraembryonic tissues and determines gene expression patterns required for normal trophoblast differentiation.
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Ovarian hyperstimulation inhibits embryo implantation in the mouse.

TL;DR: The data suggest that, in the mouse, ovarian hyperstimulation impedes implantation by causing adverse changes in uterine receptivity.
Journal ArticleDOI

Prenatal diagnosis of fetal growth restriction.

TL;DR: This chapter will discuss the various aetiologies of small fetuses and will provide the reader with diagnostic tools to distinguish between subtypes and help clinicians manage both conditions in the same way.
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