Dietary and Lifestyle Factors of DNA Methylation

Lim, Unhee; Song, Min-Ae

doi:10.1007/978-1-61779-612-8_23

Cited by 181 publications

(135 citation statements)

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“…Methylation of cytosine to 5-methyl cytosine (5mC) is considered as one of the major epigenetic modification; methylation of the CpG islands, a CG rich region in the promoter of many genes, changes protein-DNA interactions leading to alterations in chromatin structure, and this interferes with the binding of transcriptional machinery, resulting in gene suppression [17,18]. The hypomethylated DNA re-activates the repetitive genomic sequences, resulting in chromosomal instability and abnormal gene expression [19,20].…”

Section: Epigenetics and Gene Regulationmentioning

confidence: 99%

“…DNA methylation, an important epigenetic modification, is closely associated with the regulation of gene transcription [17,18]. A case control study using patients having type 2 diabetes has shown significantly higher levels of global DNA methylation in patients having diabetes with retinopathy compared to those with no retinopathy, and although global DNA methylation appears to be independent of retinopathy risk factors, e.g., hyperglycemia, dyslipidemia and hypertension, in these patients, the methylation status of DNA shows a correlation with the progression of retinopathy [63,64].…”

Section: Epigenetic Modification and Diabetesmentioning

confidence: 99%

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Contribution of epigenetics in diabetic retinopathy

Kowluru

Mishra

2015

Sci. China Life Sci.

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Diabetes has become the epidemic of the 21st century, and with over 90% patients with diabetes becoming at a risk of developing retinopathy, diabetic retinopathy has emerged as a major public health concern. In spite of cutting edge research in the field, how retina and its vasculature are damaged by the diabetic milieu remains ambiguous. The environmental factors, life style or disease process can also bring in modifications in the DNA, and these epigenetic modifications either silence or activate a gene without altering the DNA sequence. Diabetic environment up-or downregulates a number of genes in the retina, and emerging research has shown that it also facilitates epigenetic modifications. In the pathogenesis of diabetic retinopathy, the genes associated with important enzymes (e.g., mitochondrial superoxide dismutase, matrix metalloproteinase-9 and thioredoxin interacting protein) and transcriptional factors are epigenetically modified, the enzymes responsible for these epigenetic modifications are either activated or inhibited, and the levels of microRNAs are altered. With epigenetic modifications taking an important place in diabetic retinopathy, it is now becoming critical to evaluate these modifications, and understand their impact on this slow progressing blinding disease. diabetic retinopathy, epigenetic modifications, histone acetylation, histone methylation, miRNA Citation:Kowluru RA, Mishra M. Contribution of epigenetics in diabetic retinopathy.

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Section: Epigenetics and Gene Regulationmentioning

confidence: 99%

Section: Epigenetic Modification and Diabetesmentioning

confidence: 99%

Contribution of epigenetics in diabetic retinopathy

Kowluru

Mishra

2015

Sci. China Life Sci.

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“…DNA methylation has been linked to dietary, psychological, and environmental factors. (2,3) Thus, it is conceivable that postoperatively patients with HCC or CC would face changes in dietary, psychological, and environmental factors such as B vitamins, oxidative stress, and radiation. (4)(5)(6) Therefore, all these factors should be taken into account when the outcome of patients with HCC or CC is assessed, and univariate and multivariate (i.e., Cox proportional hazards model) analyses should be applied.…”

Section: To the Editormentioning

confidence: 99%

“…(2,3) Regarding the remark that biological samples differ in neoplastic cell enrichment and that DNA methylation is tissue-specific, this is surely correct. As for testing DNA methylation from blood samples, it should be pointed out that, in the present study, we measured methylation from peripheral blood mononuclear cell DNA and not from DNA obtained from circulating blood.…”

Section: Replymentioning

confidence: 99%

Hypomethylation and hypohydroxymethylation of DNA in hepatocellular carcinoma and cholangiocarcinoma

Feng

Sun

2015

Hepatology

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Hypomethylation and Hypohydroxymethylation of DNA in Hepatocellular Carcinoma and Cholangiocarcinoma TO THE EDITOR:We read with great interest the article by Udali et al.,who demonstrated that there was significantly reduced DNA methylation in hepatocellular carcinoma (HCC) compared to cholangiocarcinoma (CC) and that there was no difference in DNA hydroxymethylation between HCC and CC. They also reported that high levels of methylcytosine (mCyt) in the DNA of peripheral blood mononuclear cells (PBMCs) were related to a better clinical outcome of patients with HCC or CC. We appreciate their findings and would like to address a few issues that may help to further clarify or interpret their findings. First, methylation and hydroxymethylation of DNA play important parts in cell differentiation, embryonic development, host adaptations to environmental factors, and pathogenesis. Cytosine methylation is a DNA modification that is, in general, associated with transcriptional silencing. DNA methylation has been linked to dietary, psychological, and environmental factors.(2,3) Thus, it is conceivable that postoperatively patients with HCC or CC would face changes in dietary, psychological, and environmental factors such as B vitamins, oxidative stress, and radiation.(4-6) Therefore, all these factors should be taken into account when the outcome of patients with HCC or CC is assessed, and univariate and multivariate (i.e., Cox proportional hazards model) analyses should be applied. In addition, it should be noted that detection of the content of mCyt and hydroxymethylcytosine in the DNA of PBMCs is not practical and feasible in the clinical setting, and a surrogate parameter that is more clinically measurable would be more useful.Second, biological samples differ in accessibility and enrichment in tumor cells, as well as organ specificity, among studies on DNA methylation. Blood samples are commonly used in studies on DNA methylation, but aberrant DNA methylation can originate in any organ. How a blood-positive screening assay could point a clinician toward the site of malignancy is challenging.(7) For example, neoplastic tissues from patients with HCC or CC may contain various amounts of DNA with tissue-specific patterns of DNA methylation. Udali et al.(1) measured the global levels of mCyt and hydroxymethylcytosine in HCC and CC tissues and in DNA from PBMCs to define methylation and hydroxymethylation. They found that whereas global methylation and hydroxymethylation in DNA from PBMCs did not differ between HCC and CC, the mCyt content in HCC tissues was significantly lower than that in CC tissues. This observation clearly indicates that tissue-specific DNA methylation, not global methylation in DNA from PBMCs, plays the crucial role in differentiating between HCC and CC; and it is the tissue-specific DNA methylation (i.e., mCyt levels) that should be used as the clinical diagnostic biomarker that differentiates HCC from CC. Third, the authors followed up the 42 patients (26 HCC and 16 CC) for 48 months to assess surv...

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“…Recent technological developments now permit the precise quantification of methylation on a locus-specific level, or on a genome-wide scale. However, DNA methylation is subject to variation according to factors such as cell and tissue type, genotype, gender, age, stress, alcohol, and drug consumption [Morris et al, 2011;Bleich et al, 2006;Christensen et al, 2009;Cordero et al, 2013;Horvath, 2013;Lim and Song, 2012;Liu et al, 2010a;Liu et al, 2010b;Philibert et al, 2008;Kerkel et al, 2008]. Distinguishing cause from effect is therefore challenging in studies that find links between DNA methylation and human traits, while studies must also be interpreted within the context of the specific tissue being analyzed, and with consideration of potentially confounding variables.…”

Section: Introductionmentioning

confidence: 99%

Hypomethylation of the paternally inherited LRRTM1 promoter linked to schizophrenia

Brucato

DeLisi

Fisher

et al. 2014

American J of Med Genetics Pt B

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Epigenetic effects on psychiatric traits remain relatively understudied, and it remains unclear what the sizes of individual epigenetic effects may be, or how they vary between different clinical populations. The gene LRRTM1 (chromosome 2p12) has previously been linked and associated with schizophrenia in a parent-of-origin manner in a set of affected siblings (LOD ¼ 4.72), indirectly suggesting a disruption of paternal imprinting at this locus in these families. From the same set of siblings that originally showed strong linkage at this locus, we analyzed 99 individuals using 454-bisulfite sequencing, from whole blood DNA, to measure the level of DNA methylation in the promoter region of LRRTM1. We also assessed seven additional loci that would be informative to compare. Paternal identity-by-descent sharing at LRRTM1, within sibling pairs, was linked to their similarity of methylation at the gene's promoter. Reduced methylation at the promoter showed a significant association with schizophrenia. Sibling pairs concordant for schizophrenia showed more similar methylation levels at the LRRTM1 promoter than diagnostically discordant pairs. The alleles of common SNPs spanning the locus did not explain this epigenetic linkage, which can therefore be considered as largely independent of DNA sequence variation and would not be detected in standard genetic association analysis. Our data suggest that hypomethylation at the LRRTM1 promoter, particularly of the paternally inherited allele, was a risk factor for the development of schizophrenia in this set of siblings affected with familial schizophrenia, and that had previously showed linkage at this locus in an affected-sib-pair context. Ó 2014 Wiley Periodicals, Inc.Key words: epigenetics; parental imprint; sibling pair; psychosis INTRODUCTIONThe complex etiology of schizophrenia involves multiple environmental and genetic factors [Insel, 2010]. Epigenetic variation may also be involved, including DNA methylation [Nishioka et al., 2012], which has long been of interest in psychiatric diseases due to a role in gene regulation, and its potential to transduce environmental and genetic effects at the molecular level [Bernstein et al., 2007;Feil and Fraga, 2011]. Mainly located on cytosine bases of DNA [Bernstein et al., 2007], the role of methylation has been particularly studied in the context of gene promoters, where it can interfere with transcription [Jones, 2012;Zhang et al., 2013]. Recent technological developments now permit the precise quantification of methylation on a locus-specific level, or on a genome-wide scale. However, DNA methylation is subject to variation according to factors such as cell and tissue type, genotype, gender, age, stress, alcohol, and drug consumption [Morris et al., 2011;Bleich et al., 2006;Christensen et al., 2009;Cordero et al., 2013;Horvath, 2013;Lim and Song, 2012; Liu et al., 2010a; Liu et al., 2010b;Philibert et al., 2008;Kerkel et al., 2008]. Distinguishing cause from effect is therefore challenging in studies that find links between...

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Dietary and Lifestyle Factors of DNA Methylation

Cited by 181 publications

References 76 publications

Contribution of epigenetics in diabetic retinopathy

Contribution of epigenetics in diabetic retinopathy

Hypomethylation and hypohydroxymethylation of DNA in hepatocellular carcinoma and cholangiocarcinoma

Hypomethylation of the paternally inherited LRRTM1 promoter linked to schizophrenia

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