Placental 5-methylcytosine and 5-hydroxymethylcytosine patterns associate with size at birth

Piyasena, Chinthika; Reynolds, Rebecca M.; Khulan, Batbayar; Seckl, Jonathan R.; Menon, Gopi; Drake, Amanda J.

doi:10.1080/15592294.2015.1062963

Cited by 18 publications

(15 citation statements)

References 44 publications

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“…In contrast, the unmethylated maternal ICR1 activates H19 expression. The placenta from women diagnosed with FGR showed significantly enhanced expression of H19 and decreased methylation in its promoter, which is consistent with a notion that H19 produces an untranslated RNA that suppresses growth (Koukoura et al 2011b, Piyasena et al 2015. Although DNA methylation at ICR1 is proven to affect IGF2 expression, the methylation level at ICR1 is not significantly reduced in FGR placentas (Guo et al 2008, Bourque et al 2010.…”

Section: R234supporting

confidence: 71%

“…5-Methylcytosine (5mC) enrichment at IGF2 DMR0 and KvDMR, a CpG island located on CDKN1C gene, was independently and positively related to birth weight. 5-hydroxymethylcytosine (5hmC) enrichment within the H19 gene body was also positively related to birth weight, although no significant relationship was found at any of the regions between the mRNA levels of IGF2 and CDKN1C and 5mC or 5hmC (Piyasena et al 2015). The H19 imprinted gene clustered with the IGF2 gene on human chromosome 11p15.5, is co-controlled with IGF2 by differential methylation at an imprinting control region ICR1, located between IGF2 and H19.…”

Section: R234mentioning

confidence: 99%

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Progress in the understanding of the etiology and predictability of fetal growth restriction

Tang

Liu

et al. 2017

Reproduction

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Fetal growth restriction (FGR) is defined as the failure of fetus to reach its growth potential for various reasons, leading to multiple perinatal complications and adult diseases of fetal origins. Shallow extravillous trophoblast (EVT) invasion-induced placental insufficiency and placental dysfunction are considered the main reasons for idiopathic FGR. In this review, first we discuss the major characteristics of anti-angiogenic state and the pro-inflammatory bias in FGR. We then elaborate major abnormalities in placental insufficiency at molecular levels, including the interaction between decidual leukocytes and EVT, alteration of miRNA expression and imprinted gene expression pattern in FGR. Finally, we review current animal models used in FGR, an experimental intervention based on animal models and the progress of predictive biomarker studies in FGR. Free Chinese abstract: A Chinese translation of this abstract is freely available at http://www.reproduction-online.org/content/153/6/ R227/suppl/DC1. Reproduction (2017) 153 R227-R240

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Section: R234supporting

confidence: 71%

Section: R234mentioning

confidence: 99%

Progress in the understanding of the etiology and predictability of fetal growth restriction

Tang

Liu

et al. 2017

Reproduction

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“…Epigenetic variance or aberrant gestational dynamics may alter transcriptional output, affecting birth weight and pregnancy outcomes. Among these, targeted analysis of both 5 mC and 5hmC within the imprinted H19/IGF2 domain highlights a potential link to infant birth weight [28,29]. However, at the genome-wide level, very little is known about the distribution and function of placental 5hmC.…”

Section: Discussionmentioning

confidence: 99%

Profiling of oxBS-450K 5-hydroxymethylcytosine in human placenta and brain reveals enrichment at imprinted loci

et al. 2018

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DNA methylation (5-methylcytosine, 5 mC) is involved in many cellular processes and is an epigenetic mechanism primarily associated with transcriptional repression. The recent discovery that 5 mC can be oxidized to 5-hydromethylcytosine (5hmC) by TET proteins has revealed the "sixth base" of DNA and provides additional complexity to what was originally thought to be a stable repressive mark. However, our knowledge of the genome-wide distribution of 5hmC in different tissues is currently limited. Here, we sought to define loci enriched for 5hmC in the placenta genome by combining oxidative bisulphite (oxBS) treatment with high-density Illumina Infinium HumanMethylation450 methylation arrays and to compare our results with those obtained in brain. Despite identifying over 17,000 high-confidence CpG sites with consistent 5hmC enrichment, the distribution of this modification in placenta is relatively sparse when compared to cerebellum and frontal cortex. Supported by validation using allelic T4 β-glucosyltransferase assays we identify 5hmC at numerous imprinted loci, often overlapping regions associated with parent-of-origin allelic 5 mC in both placenta and brain samples. Furthermore, we observe tissue-specific monoallelic enrichment of 5hmC overlapping large clusters of imprinted snoRNAs-miRNAs processed from long noncoding RNAs (lncRNAs) within the DLK1-DIO3 cluster on chromosome 14 and SNRPN-UBE3A domain on chromosome 15. Enrichment is observed solely on the transcribed alleles suggesting 5hmC is positively associated with transcription at these loci. Our study provides an extensive description of the 5hmC/5 mC landscape in placenta with our data available at www.humanimprints.net , which represents the most comprehensive resource for exploring the epigenetic profiles associated with human imprinted genes.

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“…Gene expression within the placenta is recognized to be regulated, in part, by epigenetic modifications, including DNA methylation (17), and there is a growing body of literature on the impact of various environmental factors on placental DNA methylation and of placental methylation on child health outcomes (18, 19). Among these, targeted analysis of placental hydroxymethylation within the H19 imprinted gene region highlighted a potential link to infant birth weight (20). However, there is still a gap in our understanding of both the distribution and function of placental 5hmC at an epigenome‐wide level.…”

mentioning

confidence: 99%

Hydroxymethylation is uniquely distributed within term placenta, and is associated with gene expression

et al. 2016

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The conversion of cytosine to 5-methylcystosine (5mC) is an important regulator of gene expression. 5mC may be enzymatically converted to 5-hydroxymethylcytosine (5hmC), with a potentially distinct regulatory function. We sought to investigate these cytosine modifications and their effect on gene expression by parallel processing of genomic DNA using bisulfite and oxidative bisulfite conversion in conjunction with RNA sequencing. Although values of 5hmC across the placental genome were generally low, we identified ∼21,000 loci with consistently elevated levels of 5-hydroxymethycytosine. Absence of 5hmC was observed in CpG islands and, to a greater extent, in non-CpG island-associated regions. 5hmC was enriched within poised enhancers, and depleted within active enhancers, as defined by H3K27ac and H3K4me1 measurements. 5hmC and 5mC were significantly elevated in transcriptionally silent genes when compared with actively transcribed genes. 5hmC was positively associated with transcription in actively transcribed genes only. Our data suggest that dynamic cytosine regulation, associated with transcription, provides the most complete epigenomic landscape of the human placenta, and will be useful for future studies of the placental

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Placental 5-methylcytosine and 5-hydroxymethylcytosine patterns associate with size at birth

Abstract: (2015) Placental 5-methylcytosine and 5-hydroxymethylcytosine patterns associate with size at birth, Epigenetics, 10:8,[692][693][694][695][696][697]

Cited by 18 publications

References 44 publications

Progress in the understanding of the etiology and predictability of fetal growth restriction

Progress in the understanding of the etiology and predictability of fetal growth restriction

Profiling of oxBS-450K 5-hydroxymethylcytosine in human placenta and brain reveals enrichment at imprinted loci

Hydroxymethylation is uniquely distributed within term placenta, and is associated with gene expression

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