Epigenetics of Inflammatory Bowel Disease: Unraveling Pathogenic Events

Mateos, Beatriz; Palanca-Ballester, Cora; Saéz-González, Esteban; Moret, Inés; López, Adrián Valdrés; Sandoval, Juan

doi:10.1093/crocol/otz017

Cited by 6 publications

(6 citation statements)

References 15 publications

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“…The major epigenetic mechanisms that control gene expression are DNA methylation, histone modifications (such as acetylation and methylation), and small, non-coding RNAs. Epigenetic mechanisms are dynamic, reversible, and influenced by exposure to environmental factors [ 115 ]. Given that these mechanisms are involved in proper cell development, differentiation, function, and homeostasis, their dysregulation is proposed to play a key role in the onset and development of several diseases, especially cancer [ 116 ].…”

Section: The Role Of the Environment In Crohn’s Diseasementioning

confidence: 99%

“…Epigenetic mechanisms, especially DNA methylation and microRNA expression, are identified as dysregulated in CD and are proposed as candidate biomarkers of the disease [ 115 ]. DNA methylation is the most studied epigenetic modification and consists of the covalent addition of a methyl group to the 5′ carbon of the cytosine ring, in the context of CpG dinucleotides.…”

Section: The Role Of the Environment In Crohn’s Diseasementioning

confidence: 99%

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Oxidative Stress in the Pathogenesis of Crohn’s Disease and the Interconnection with Immunological Response, Microbiota, External Environmental Factors, and Epigenetics

et al. 2021

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Inflammatory bowel disease (IBD) is a complex multifactorial disorder in which external and environmental factors have a large influence on its onset and development, especially in genetically susceptible individuals. Crohn’s disease (CD), one of the two types of IBD, is characterized by transmural inflammation, which is most frequently located in the region of the terminal ileum. Oxidative stress, caused by an overabundance of reactive oxygen species, is present locally and systemically in patients with CD and appears to be associated with the well-described imbalanced immune response and dysbiosis in the disease. Oxidative stress could also underlie some of the environmental risk factors proposed for CD. Although the exact etiopathology of CD remains unknown, the key role of oxidative stress in the pathogenesis of CD is extensively recognized. Epigenetics can provide a link between environmental factors and genetics, and numerous epigenetic changes associated with certain environmental risk factors, microbiota, and inflammation are reported in CD. Further attention needs to be focused on whether these epigenetic changes also have a primary role in the pathogenesis of CD, along with oxidative stress.

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Section: The Role Of the Environment In Crohn’s Diseasementioning

confidence: 99%

Section: The Role Of the Environment In Crohn’s Diseasementioning

confidence: 99%

Oxidative Stress in the Pathogenesis of Crohn’s Disease and the Interconnection with Immunological Response, Microbiota, External Environmental Factors, and Epigenetics

et al. 2021

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“…These diseases have unknown etiology, and there is insufficient information about pathogenesis, but it is believed that a complex interaction of genetic, epigenetic, microbial, environmental and immunological factors are involved [ 137 ]. In particular, several studies have evaluated the epigenetic status of IBD patients using candidate gene strategies [ 138 , 139 , 140 , 141 , 142 ] or epigenome-wide association studies [ 143 , 144 , 145 , 146 ], trying to elucidate IBD pathogenesis [ 147 ]. Cooke and colleagues [ 143 ] collected rectal biopsies and identified some glycogenes that have a differential methylation status between patients with CD and UC (inflamed vs. non-inflamed) and healthy controls.…”

Section: Epigenetic Regulation Of Glycosylation In Other Diseasesmentioning

confidence: 99%

Epigenetic Regulation of Glycosylation in Cancer and Other Diseases

Indellicato

Trinchera

2021

IJMS

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In the last few decades, the newly emerging field of epigenetic regulation of glycosylation acquired more importance because it is unraveling physiological and pathological mechanisms related to glycan functions. Glycosylation is a complex process in which proteins and lipids are modified by the attachment of monosaccharides. The main actors in this kind of modification are the glycoenzymes, which are translated from glycosylation-related genes (or glycogenes). The expression of glycogenes is regulated by transcription factors and epigenetic mechanisms (mainly DNA methylation, histone acetylation and noncoding RNAs). This review focuses only on these last ones, in relation to cancer and other diseases, such as inflammatory bowel disease and IgA1 nephropathy. In fact, it is clear that a deeper knowledge in the fine-tuning of glycogenes is essential for acquiring new insights in the glycan field, especially if this could be useful for finding novel and personalized therapeutics.

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“…Genome-wide association studies (GWAS) have made it clear that genetics alone does not fully explain heritability in CD [3][4][5]. As such, CD has been classified as a complex disorder whose etiology is likely to be a combination of genetic [4], epigenetic [6,7] and other environmental factors. Epigenetics pertain to mitotically heritable changes that affect the readability of the genome that are not caused by changes to the genetic sequence.…”

Section: Introductionmentioning

confidence: 99%

Whole-Genome DNA Methylation Profiling of CD14+ Monocytes Reveals Disease Status and Activity Differences in Crohn’s Disease Patients

Yim

Duijvis

Ghiboub

et al. 2020

JCM

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Crohn’s disease (CD) is a multifactorial incurable chronic disorder. Current medical treatment seeks to induce and maintain a state of remission. During episodes of inflammation, monocytes infiltrate the inflamed mucosa whereupon they differentiate into macrophages with a pro-inflammatory phenotype. Here, we sought to characterize the circulating monocytes by profiling their DNA methylome and relate it to the level of CD activity. We gathered an all-female age-matched cohort of 16 CD patients and 7 non-CD volunteers. CD patients were further subdivided into 8 CD patients with active disease (CD-active) and 8 CD patients in remission (CD-remissive) as determined by the physician global assessment. We identified 15 and 12 differentially methylated genes (DMGs) when comparing CD with non-CD and CD-active with CD-remissive, respectively. Differential methylation was predominantly found in the promoter regions of inflammatory genes. Comparing our observations with gene expression data on classical (CD14++CD16-), non-classical (CD14+CD16++) and intermediate (CD14++CD16+) monocytes indicated that while 7 DMGs were differentially expressed across the 3 subsets, the remaining DMGs could not immediately be associated with differences in known populations. We conclude that CD activity is associated with differences in DNA methylation at the promoter region of inflammation-associated genes.

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Epigenetics of Inflammatory Bowel Disease: Unraveling Pathogenic Events

Cited by 6 publications

References 15 publications

Oxidative Stress in the Pathogenesis of Crohn’s Disease and the Interconnection with Immunological Response, Microbiota, External Environmental Factors, and Epigenetics

Oxidative Stress in the Pathogenesis of Crohn’s Disease and the Interconnection with Immunological Response, Microbiota, External Environmental Factors, and Epigenetics

Epigenetic Regulation of Glycosylation in Cancer and Other Diseases

Whole-Genome DNA Methylation Profiling of CD14+ Monocytes Reveals Disease Status and Activity Differences in Crohn’s Disease Patients

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