Review¶Hormone action and chromatin remodelling

Robyr, Daniel; Wolffe, Alan P.

doi:10.1007/s000180050130

Cited by 17 publications

(4 citation statements)

References 133 publications

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“…Steroids are routinely administered to women in preterm labor due to known improved outcomes in preterm infants, especially in accelerating lung maturation. 31 Glucocorticoids have been shown to alter DNA methylation, 32,33 thus representing a putative modifier of the offspring epigenome that may explain the long-term consequences of the antenatal glucocorticoid exposure on neurologic, cardiovascular, and metabolic function. 19 In our studies, treating pregnant mice with dexamethasone resulted in major gene expression changes in the tight junction and toll-like receptor associated pathways of the offspring, associated with alterations in the microbiome.…”

Section: Discussionmentioning

confidence: 99%

Epigenome-Microbiome crosstalk: A potential new paradigm influencing neonatal susceptibility to disease

et al. 2016

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Preterm birth is the leading cause of infant morbidity and mortality. Necrotizing enterocolitis (NEC) is an inflammatory bowel disease affecting primarily premature infants, which can be lethal. Microbial intestinal colonization may alter epigenetic signatures of the immature gut establishing inflammatory and barrier properties predisposing to the development of NEC. We hypothesize that a crosstalk exists between the epigenome of the host and the initial intestinal colonizing microbiota at critical neonatal stages. By exposing immature enterocytes to probiotic and pathogenic bacteria, we showed over 200 regions of differential DNA modification, which were specific for each exposure. Reciprocally, using a mouse model of prenatal exposure to dexamethasone we demonstrated that antenatal treatment with glucocorticoids alters the epigenome of the host. We investigated the effects on the expression profiles of genes associated with inflammatory responses and intestinal barrier by qPCR-based gene expression array and verified the DNA modification changes in 5 candidate genes by quantitative methylation specific PCR (qMSP). Importantly, by 16S RNA sequencing-based phylogenetic analysis of intestinal bacteria in mice at 2 weeks of life, we showed that epigenome changes conditioned early microbiota colonization leading to differential bacterial colonization at different taxonomic levels. Our findings support a novel conceptual framework in which epigenetic changes induced by intrauterine influences affect early microbial colonization and intestinal development, which may alter disease susceptibility.

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Section: Discussionmentioning

confidence: 99%

Epigenome-Microbiome crosstalk: A potential new paradigm influencing neonatal susceptibility to disease

et al. 2016

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“…Generally, these involve alterations to chromatin structure or to mRNA transcription and translation. Hormones, such as the glucocorticoids, have been shown to alter DNA methylation, particularly at the GR promotor (Robyr & Wolffe, 1998; Adcock et al 2004). In cultured hepatocytes from fetal rats, dexamethasone induces stable DNA demethylation at the glucocorticoid response element of the tyrosine aminotransferase gene, which is associated with increased expression of this gene (Thomassin et al 2001).…”

Section: Molecular Mechanisms By Which Hormones Act On Phenotypementioning

confidence: 99%

“…Changes in methylation status induced in utero may persist after birth to alter adult gene expression, since demethylation of the GR promotor and increased GR gene expression have been observed in kidneys of adult rats overexposed to glucocorticoids during late gestation (Wyrwoll et al 2007). Relatively little is known about the effects of hormones on histone modifications during early development, although histone acetylation is hormone sensitive in adult tissues and can be altered in fetal liver and brain by conditions, such as maternal dietary manipulation and uteroplacental insufficiency, which affect the fetal endocrine environment (Robyr & Wolffe, 1998; Fu et al 2004; Ke et al 2006; Aagaard‐Tillery et al 2008). Even less is known about the endocrine regulation of the DNA methyltransferases responsible for the maintenance and de novo methylation of DNA during development.…”

Section: Molecular Mechanisms By Which Hormones Act On Phenotypementioning

confidence: 99%

Hormones as epigenetic signals in developmental programming

Fowden

Forhead

2009

Experimental Physiology

114

120

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In mammals, including man, epidemiological and experimental studies have shown that a range of environmental factors acting during critical periods of early development can alter adult phenotype. Hormones have an important role in these epigenetic modifications and can signal the type, severity and duration of the environmental cue to the developing feto-placental tissues. They affect development of these tissues both directly and indirectly by changes in placental phenotype. They act to alter gene expression, hence the protein abundance in a wide range of different tissues, which has functional consequences for many physiological systems both before and after birth. By producing an epigenome specific to the prevailing condition in utero, hormones act as epigenetic signals in developmental programming, with important implications for adult health and disease. This review examines the role of hormones as epigenetic signals by considering their responses to environmental cues, their effects on phenotypical development and the molecular mechanisms by which they programme feto-placental development, with particular emphasis on the glucocorticoids.

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“…Many of these accessory molecules, also termed co-regulators, act to modify the chromatin structure at the response element and within the promoter of target genes (Trotter and Archer, 2008, Wolf, Heitzer, Grubisha et al, 2008). It has become abundantly clear that biology uses that chromatin structure and the ability to modify it as an important step in regulating transcription factor function (Robyr and Wolffe, 1998). …”

Section: Introductionmentioning

confidence: 99%

Chromatin architecture defines the glucocorticoid response

Burd

Archer

2013

Molecular and Cellular Endocrinology

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The glucocorticoid receptor (GR) functions to regulate a wide group of physiological processes through hormone inducible interaction with genomic loci and subsequent manipulation of the transcriptional output of target genes. Despite expression in a wide variety of tissues, the GR has diverse roles that are regulated tightly in a cell type specific manner. With the advent of whole genome approaches, the details of that diversity and the mechanisms regulating them are beginning to be elucidated. This review aims describe the recent advances detailing the role chromatin structure plays in dictating GR specificity.

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Review¶Hormone action and chromatin remodelling

Cited by 17 publications

References 133 publications

Epigenome-Microbiome crosstalk: A potential new paradigm influencing neonatal susceptibility to disease

Epigenome-Microbiome crosstalk: A potential new paradigm influencing neonatal susceptibility to disease

Hormones as epigenetic signals in developmental programming

Chromatin architecture defines the glucocorticoid response

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