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.read more
Citations
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Role of Tet1 in erasure of genomic imprinting
TL;DR: Analysis of the DNA methylation dynamics in reprograming PGCs indicates that Tet1 functions to wipe out remaining methylation, including imprinted genes, at the late reprogramming stage, establishing a critical function of Tet1 in the erasure of genomic imprinting.
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Placental contribution to nutritional programming of health and diseases: epigenetics and sexual dimorphism.
TL;DR: The aim of this review is to discuss the emerging knowledge on the relationships between the effect of maternal nutrition or metabolic status on placental function and the risk of diseases later in life, with a specific focus on epigenetic mechanisms and sexual dimorphism.
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Single-cell RNA-seq reveals the diversity of trophoblast subtypes and patterns of differentiation in the human placenta
Ya-Wei Liu,Xiaoying Fan,Rui Wang,Xiaoyin Lu,Xiaoyin Lu,Yan-Li Dang,Huiying Wang,Hai-Yan Lin,Cheng Zhu,Hao Ge,James C. Cross,Hongmei Wang +11 more
TL;DR: Functionally, this study revealed many previously unknown functions of the human placenta, and 102 polypeptide hormone genes were found to be expressed by various subtypes of placental cells, which suggests a complex and significant role of these hormones in regulating fetal growth and adaptations of maternal physiology to pregnancy.
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In utero exposures, infant growth, and DNA methylation of repetitive elements and developmentally related genes in human placenta.
Charlotte Wilhelm-Benartzi,E. Andres Houseman,Matthew A. Maccani,Graham M. Poage,Devin C. Koestler,Scott M. Langevin,Luc Gagne,Carolyn E. Banister,James F. Padbury,Carmen J. Marsit +9 more
TL;DR: The results suggest that repetitive element methylation markers, most notably AluYb8 methylation, may be susceptible to epigenetic alterations resulting from the intrauterine environment and play a critical role in mediating placenta function, and may ultimately inform on the developmental basis of health and disease.
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Epigenetic Mechanisms of Transmission of Metabolic Disease across Generations
TL;DR: This Perspective focuses on epigenetic mechanisms in germ cells, including DNA methylation, histone modification, and non-coding RNAs, which collectively may provide a non-genetic molecular legacy of prior environmental exposures and influence transcriptional regulation, developmental trajectories, and adult disease risk in offspring.
References
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DNA methylation patterns and epigenetic memory
TL;DR: The heritability of methylation states and the secondary nature of the decision to invite or exclude methylation support the idea that DNA methylation is adapted for a specific cellular memory function in development.
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DNA methyltransferases Dnmt3a and Dnmt3b are essential for de novo methylation and mammalian development.
TL;DR: It is demonstrated that two recently identified DNA methyltransferases, DnMT3a and Dnmt3b, are essential for de novo methylation and for mouse development and play important roles in normal development and disease.
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Vitamin D
TL;DR: In what case do you like reading so much? What about the type of the vitamin d the calcium homeostatic steroid hormone book? The needs to read? Well, everybody has their own reason why should read some books as discussed by the authors.
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Targeted mutation of the DNA methyltransferase gene results in embryonic lethality.
TL;DR: Results indicate that while a 3-fold reduction in levels of genomic m5C has no detectable effect on the viability or proliferation of ES cells in culture, a similar reduction of DNA methylation in embryos causes abnormal development and embryonic lethality.
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The Transcriptional Landscape of the Mammalian Genome
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TL;DR: Detailed polling of transcription start and termination sites and analysis of previously unidentified full-length complementary DNAs derived from the mouse genome provide a comprehensive platform for the comparative analysis of mammalian transcriptional regulation in differentiation and development.