Epigenetics of inflammatory bowel disease

Petronis, Artūras; Petronienė, Rima

doi:10.1136/gut.47.2.302

Cited by 46 publications

(38 citation statements)

References 80 publications

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“…Namely, recent epigenetic studies provide evidence that during gametogenesis, development, and aging, heritable modifications in gene expression occur due to potentially reversible changes in DNA methylation and/or chromatin structure (Pikaard 2000;Mechali 2001). These mechanisms have been hypothesized in human inflammatory and psychiatric disorders (Petronis and Petroniene 2000; and we acknowledge that they may account for diverse subphenotypes in inbred MRL-lpr animals. At the same time, we take the point that they do not negate a principal role of systemic autoimmune processes in affecting brain morphology and function.…”

Section: Discussionmentioning

confidence: 79%

Behavioral heterogeneity in an animal model of neuropsychiatric lupus

Šakić¹,

Hanna²,

Millward³

2005

Biological Psychiatry

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Background-Various psychiatric manifestations of unknown etiology are common in systemic autoimmune disease lupus erythematosus (SLE). Profound heterogeneity at clinical and neuropathological levels suggests distinct subpopulations of SLE patients and multiple mechanisms in the pathogenesis of aberrant behavior. Using inbred mice prone to SLE-like condition, we presently examine whether subpopulations of diseased mice can be identified on the basis of their behavioral performance.

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Section: Discussionmentioning

confidence: 79%

Behavioral heterogeneity in an animal model of neuropsychiatric lupus

Šakić¹,

Hanna²,

Millward³

2005

Biological Psychiatry

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“…It has been proposed that epigenetic factors play an important role in the pathogenesis of IBD, 37 and that sex effects are mediated by androgens and oestrogens. Hormones have a substantial effect on gene expression, and the hormonal differences between males and females could thus lead to differential expression of disease susceptibility genes in males and females.…”

Section: 29mentioning

confidence: 99%

Sex stratification of an inflammatory bowel disease genome search shows male-specific linkage to the HLA region of chromosome 6

et al. 2002

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Inflammatory bowel disease (IBD) is a multifactorial disorder, with both genetic and environmental factors contributing to the two clinical phenotypes of Crohn's disease (CD) and ulcerative colitis (UC). The underlying genetic model is thought to involve multiple genes with complex interactions between disease loci, and the NOD2 gene on chromosome 16 has recently been identified as a CD susceptibility locus. Several genome-wide linkage studies have identified candidate regions, but there has been little replication across studies. Here we investigate the role of sex-specific loci in susceptibility to IBD. Linkage data from our previously reported genome search and follow-up study were stratified by the sex of the affected sib pair. Non-parametric linkage analysis was performed using Genehunter Plus. Simulation studies were used to assess the significance of differences in LOD scores between male and female families for each chromosome. Several regions of sex-specific linkage were identified, including existing and novel candidate loci. The major histocompatibility region on chromosome 6p, referred to as IBD3, showed evidence of male-specific linkage with a maximum LOD score of 5.9 in both CD and UC male-affected families. Regions on chromosomes 11, 14 and 18 showed strong evidence of linkage in male-affected families but not in female-affected families. No evidence of sex-specific linkage was found in the IBD1 or IBD2 candidate regions of chromosomes 16 and 12. The existence of sex-specific linkage is further evidence of the complex mechanisms involved in IBD and will facilitate future studies to identify susceptibility genes.

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“…Since epigenetic changes can also be detected in precancerous lesions tissues (Gonzalo et al, 2010) suggesting its potential role in the initial carcinogenesis (Petronis and Petroniene, 2000;Jawad, et al, 2011;Cooke, et al, 2012;Jenke and Zilbauer, 2012;Olaru, et al, 2012). Gene promoter hypermethylation in normal appearing colorectal mucosa has been suggested in the MGMT gene as well as, MLH1, TIMP3 and DAPK (Gonzalo, et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

“…methylation of genes like p16, E-cadherin, hMLH1 and p14 has been reported in IBD associated neoplasia (Dhir et al, 2008;Low et al, 2013). These epigenetic changes may accelerate the development of IBD-CRC (Petronis and Petroniene, 2000;Goel, et al, 2011;Jawad et al, 2011;Lin, et al, 2011;Jenke and Zilbauer, 2012;Kellermayer, 2012). CpG island methylation phenotype and global DNA methylation with LINE-1 assay were also observed in 17% and 58% of the ulcerative colitis (UC) related cancers, respectively (Konishi et al, 2007).…”

Section: Introductionmentioning

confidence: 99%