scispace - formally typeset
Open AccessJournal ArticleDOI

Epigenetics and the placenta

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.

read more

Citations
More filters
Journal ArticleDOI

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.
Journal ArticleDOI

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
More filters
Journal ArticleDOI

Gene Silencing in Cancer in Association with Promoter Hypermethylation

TL;DR: The mechanisms of gene silencing in cancer and clinical applications of this phenomenon are reviewed, especially tumor-suppressor genes.
Journal ArticleDOI

Epigenetic Reprogramming in Mammalian Development

TL;DR: What is known about reprogramming in mammals and how it might relate to developmental potency and imprinting are discussed, including whether or not methylation is involved in the control of gene expression during normal development.
Journal ArticleDOI

Perceptions of epigenetics

TL;DR: During the past year, more than 2,500 articles, numerous scientific meetings and a new journal were devoted to the subject of epigenetics, portrayed by the popular press as a revolutionary new science — an antidote to the idea that the authors are hard-wired by their genes.
Journal ArticleDOI

Polycomb complexes repress developmental regulators in murine embryonic stem cells

TL;DR: It is shown that PcG proteins directly repress a large cohort of developmental regulators in murine ES cells, the expression of which would otherwise promote differentiation, and dynamic repression of developmental pathways by Polycomb complexes may be required for maintaining ES cell pluripotency and plasticity during embryonic development.
Journal ArticleDOI

Type 2 (non-insulin-dependent) diabetes mellitus, hypertension and hyperlipidaemia (syndrome X): relation to reduced fetal growth

TL;DR: It is concluded that Type 2 diabetes and hypertension have a common origin in sub-optimal development in utero, and that syndrome X should perhaps be re-named “the small-baby syndrome”.
Related Papers (5)