Epigenetic regulation of the intestinal epithelium

Elliott, Ellen N.; Kaestner, Klaus H.

doi:10.1007/s00018-015-1997-9

Cited by 34 publications

(22 citation statements)

References 206 publications

(279 reference statements)

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“…In particular, morphogenesis of lung epithelial barriers continues throughout normal postnatal development, characterized by ongoing septation and epithelialization of the lung 104 . Consequently, perturbation of barrier morphogenesis in childhood may have a lasting effect on adult epithelium via alteration of developmental programs and epigenetic reprogramming at developmental checkpoints 105–107 . Multiple lines of evidence now implicate active re-engagement of morphogenetic programs in adult disease, typically not seen in adult homeostatic tissue 108–110 .…”

Section: Mechanisms Of Barrier Defectsmentioning

confidence: 99%

Etiology of epithelial barrier dysfunction in patients with type 2 inflammatory diseases

Schleimer

Berdnikovs

2017

Journal of Allergy and Clinical Immunology

134

122

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Epithelial barriers of the skin, gastrointestinal tract and airway serve common critical functions such as maintaining a physical barrier against environmental insults and allergens, as well as providing a tissue interface balancing the communication between the internal and external environments. We now understand that in allergic disease, regardless of tissue location, the homeostatic balance of the epithelial barrier is skewed towards loss of differentiation, reduced junctional integrity and impaired innate defense. Importantly, epithelial dysfunction characterized by these traits appears to pre-date atopy and development of allergic disease. Despite our growing appreciation of the centrality of barrier dysfunction in the initiation of allergic disease, many important questions remain to be answered regarding the mechanisms disrupting the normal barrier function. Although our external environment (proteases, allergens, injury) is classically thought of as a principal contributor to barrier disruption associated with allergic sensitization, there is a need to better understand contributions of the internal environment (hormones, diet, circadian clock). Systemic drivers of disease, such as alterations of the endocrine system, metabolism and aberrant control of developmental signaling, are emerging as new players in driving epithelial dysfunction and allergic predisposition at various barrier sites. Identifying such central mediators of epithelial dysfunction, using both systems biology tools and causality-driven laboratory experimentation, will be essential in building new strategic interventions to prevent or reverse the process of barrier loss in allergy.

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Section: Mechanisms Of Barrier Defectsmentioning

confidence: 99%

Etiology of epithelial barrier dysfunction in patients with type 2 inflammatory diseases

Schleimer

Berdnikovs

2017

Journal of Allergy and Clinical Immunology

134

122

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“…Recent work has suggested that microbiota-directed epigenomics is a central mechanism driving intestinal development [74,75]. Genome-wide examination of the postnatal methylome revealed microbiota-dependent increases in DNA methylation in intestinal stem cells within maturation-associated genes that positively correlated with increased gene expression [76].…”

Section: Epigenomic Pathways Directed By the Microbiota Maintain Intementioning

confidence: 99%

Host–microbiota interactions: epigenomic regulation

Woo

Alenghat

2017

Current Opinion in Immunology

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The coevolution of mammalian hosts and their commensal microbiota has led to the development of complex symbiotic relationships between resident microbes and mammalian cells. Epigenomic modifications enable host cells to alter gene expression without modifying the genetic code, and therefore represent potent mechanisms by which mammalian cells can transcriptionally respond, transiently or stably, to environmental cues. Advances in genome-wide approaches are accelerating our appreciation of microbial influences on host physiology, and increasing evidence highlights that epigenomics represent a level of regulation by which the host integrates and responds to microbial signals. In particular, bacterial-derived short chain fatty acids have emerged as one clear link between how the microbiota intersects with host epigenomic pathways. Here we review recent findings describing crosstalk between the microbiota and epigenomic pathways in multiple mammalian cell populations. Further, we discuss interesting links that suggest that the scope of our understanding of epigenomic regulation in the host-microbiota relationship is still in its infancy.

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“…According to the epigenetic progenitor model of cancer epigenetic alterations affecting tissue specific differentiation are the prominent mechanism by which epigenetic changes cause cancer . However, there is still a lack of information about the precise changes occurring in the epigenetic state during differentiation processes of the intestinal epithelium .…”

Section: Discussionmentioning

confidence: 99%

Analyzing epigenetic control of galectin expression indicates silencing of galectin‐12 by promoter methylation in colorectal cancer

et al. 2017

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Galectins, a class of lectins with specificity for ß-galactoside containing glycoconjugates, modulate several cellular processes that are involved in the control of normal cell growth, differentiation, cell-cell, and cell matrix interactions. Pathological alterations of the galectin expression pattern have been implicated in the development and progression of cancer. We therefore analyzed epigenetic mechanisms for control of galectin expression in 9 colorectal cancer (CRC) cell lines. Our data demonstrate that expression of galectins-1, -2, -7, -8, and -9 can be regulated by histone acetylation in CRC cell lines. In addition, the same set of galectins was also found to be modulated by DNA methylation. Of particular note, galectin-12 is silenced in all tested CRC cell lines but known to be re-expressed upon butyrate-induced differentiation and present in normal colonic mucosa. Loss of galectin-12 expression in undifferentiated CRC cells is associated with promoter hypermethylation and for the first time we provide detailed methylation analysis of the promoter region. In CRC tumor tissue, galectin-12 expression was downregulated in 66% of CRC tissue specimens as compared to adjacent normal tissue hinting to a possible tumor-suppressing function in CRC. © 2017 IUBMB Life, 69(12):962-970, 2017.

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Epigenetic regulation of the intestinal epithelium

Cited by 34 publications

References 206 publications

Etiology of epithelial barrier dysfunction in patients with type 2 inflammatory diseases

Etiology of epithelial barrier dysfunction in patients with type 2 inflammatory diseases

Host–microbiota interactions: epigenomic regulation

Analyzing epigenetic control of galectin expression indicates silencing of galectin‐12 by promoter methylation in colorectal cancer

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