The alteration of DNA methylation driven by HIV infection based on a pair of monozygotic twins (MeDIP-chip)
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Yinfeng Zhang
PROVIDER: E-GEOD-68028 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:In this study, we have investigated the relationship between genome-wide DNA methylation pattern and HIV infection using the methylated DNA immunoprecipitation - microarray method. A pair of monozygotic twins was recruited: one of the twins was infected with HIV while the other was not. The immunoprecipitated CpG-methylated DNA from HIV positive subject (test) and from HIV negative subject (input control) were labelled with Cy5 and Cy3 respectively
2015-04-20 | GSE68028 | GEO
Project description:Age-related macular degeneration (AMD) is the leading cause of irreversible blindness in the elderly population worldwide. Recent studies have demonstrated strong genetic associations between AMD and single nucleotide polymorphisms (SNPs) within genes such as CFH and HTRA1. However, we found monozygotic twins had discordant AMD phenotypes (one with disease, the other without disease), suggesting that an epigenetic mechanism may control the pathogenesis of AMD. We obtained genomic DNA from the twins' peripheral blood mononuclear cells (PBMCs) and subjected it to DNA methylation-chip analysis (MeDIP-chip) that profiled genome-wide DNA methylation patterns on promoters of all genes and microRNAs. Our MeDIP-chip analysis identified 256 genes with hypo-methylated promoters only in the twins with AMD and 744 genes with hyper-methylated promoters only in the twins with AMD. Importantly, the promoter region of IL17RC was associated with hypo-methylated CpG sites only in the twins with AMD but not in the twins without AMD. Two pairs of twins with discordant AMD phenotypes. MeDIP-chip analysis of DNA methylation patterns in PBMCs.
2011-03-21 | E-GEOD-28032 | biostudies-arrayexpress
Project description:To further our understanding of the role of DNA methylation in development, Methylated DNA Immunoprecipitation (MeDIP) was used in conjunction with a NimbleGen promoter plus CpG island array to identify Tissue and Developmental Stage specific Differentially Methylated DNA Regions (T-DMRs and DS-DMRs) on a genome-wide basis. Four tissues (brain, heart, liver, and testis) from C57BL/6J mice were analyzed at three developmental stages (15 day embryo, E15; new born, NB; 12 week adult, AD). Almost 5,000 adult T-DMRs and 10,000 DS-DMRs were identified. Surprisingly, almost all DS-DMRs were tissue specific (i.e., methylated and ummenthylated in one or more non-overlapping tissues), indicating that the vast majority of unique sequence DNA methylation has tissue specificity. Also, many DS-DMRs were methylated at early development stages (E15 and NB) but unmethylated in adult, indicating “demethylation” has a prominent role in tissue differentiation. The pattern of DNA methylation in adult testis was dramatically different from somatic tissues in many aspects, mostly notably with a very strong bias of methylation in non-CpGi (CpG island) promoter regions (94%). Although the majority of T-DMRs and DS-DMRs tended to be in non-CpGi promoter regions, a relatively large number were also located in CpGi in promoter, intra-genic and inter-genic regions (>15% of all CpGi). Gene Ontology analysis of genes with methylation in non-CpGi promoters indicates enrichment of genes related to membrane proteins and G-protein coupled receptors. Our data also suggest regulatory roles of DNA methylation outside of promoter regions and in alternative promoter selection. Overall, our studies indicate that change in DNA methylation during development is a dynamic, widespread and tissue-specific process involving both DNA methylation and demethylation. Comparison of DNA methylation across 3 developmental stages (15 day embryo, newborn, and adult) for four tissues (brain, heart, liver and testis)
2010-12-31 | E-GEOD-21415 | biostudies-arrayexpress
Project description:Chronic pain is a global public health problem, but the underlying molecular mechanisms are not fully understood. Here we examine genome-wide DNA methylation, first in 50 identical twins discordant for heat pain sensitivity and then in 50 further unrelated individuals. Whole blood DNA methylation was characterized at 5.2 million loci by MeDIP-sequencing and assessed longitudinally to identify differentially methylated regions associated with high or low pain-sensitivity (pain-DMRs). Nine meta-analysis pain-DMRs show robust evidence for association (false discovery rate 5%) with the strongest signal in the pain gene TRPA1 (P=1.2M-CM-^W10-13). Several pain-DMRs show longitudinal stability consistent with susceptibility effects, have similar methylation levels in brain, and altered expression in skin. Our approach identifies epigenetic changes in both novel and established candidate genes that provide molecular insights into pain and may generalize to other complex traits. MeDIP-sequencing in 100 individulas using a 2 stage design: paired-end MeDIP-seq in 50 monozygotic twins and single-end MeDIP-seq in 50 unrelated individuals.
2013-12-04 | E-GEOD-52965 | biostudies-arrayexpress
Project description:Human intelligence demonstrates one of the highest heritabilities among human quantitative traits. Phenotypically discordant monozygotic twins provide a way to identify loci reponsible for the phenotypical differences. We performed comprehensive DNA methylation analysis in monozygotic twins manifesting differences in IQ scores. Genes with significantly different methylation status are considered as candidates related to human intelligence. Methylation profiling was conducted using methylated DNA enriched fraction by MethylMiner. Subjects were compared with their co-twins by MAT software and bed files were generated. Significantly high methyalted regions with MAT score p value < 0.000001 in each twin pairs were extracted as candidates.
2012-10-20 | E-GEOD-33477 | biostudies-arrayexpress
Project description:Epigenetic regulation plays essential role in cell differentiation and dedifferentiation, which are the intrinsic processes involved in regeneration. In order to investigate the epigenetic basis of regeneration capacity, we choose DNA methylation as one of the most important epigenetic mechanisms and the MRL/MpJ mouse as a model of mammalian regeneration reported to exhibit enhanced regeneration response in different organs. We report the comparative analysis of genomic DNA methylation profiles of the MRL/MpJ and the control C57BL/6J mouse. Methylated DNA immunoprecipitation (MeDIP) followed by microarray analysis using Nimblegen M-bM-^@M-^\3x720K CpG Island Plus RefSeq PromoterM-bM-^@M-^] platform were applied in order to carry out genome-wide DNA methylation profiling covering 20,404 promoter regions. We identified hundreds of hypo- and hypermethylated genes and CpG islands in heart, liver and spleen, and 37 of them in the three tissues. Decreased inter-tissue diversification and the shift of DNA methylation balance upstream the genes distinguish the genomic methylation patterns of the MRL/MpJ mouse from the C57BL/6J. Homeobox genes and a number of other genes involved in embryonic morphogenesis are significantly over-represented among the genes hypomethylated in the MRL/MpJ mouse. These findings indicate that epigenetic patterning might be a likely molecular basis of regeneration capability in the MRL/MpJ mouse. genome-wide DNA methylation profiling in the heart, liver, and spleen tissues of MRL/MpJ and C57BL/6J mouse
2013-08-20 | E-GEOD-49221 | biostudies-arrayexpress
Project description:Early postnatal life is considered as a critical time window for determination of long-term metabolic states and organ functions. Extrauterine growth restriction (EUGR) causes the development of adult onset chronic diseases, including pulmonary arterial hypertension (PAH). However, the effects of nutritional disadvantages during early postnatal period on pulmonary vascular consequences in later life are not fully understood. Our study was designed to test whether epigentic dysregulation mediates the cellular memory of this early postnatal event. To test this hypothesis, we isolated pulmonary vascular endothelial cells (PVEC) by magnetic-activated cell sorting (MACS) from EUGR and control rats. A postnatal insult, nutritional restriction-induced EUGR caused development of an increased pulmonary artery pressure at 9-week of age in male rats. MeDIP-chip (Methyl-DNA immune precipitation chip), genome-scale mapping studies to search for differentially methylated loci between control and EUGR rats revealed significant difference in cytosine methylation between EUGR and control rats. We validated candidate dysregulated loci with quantitative assays of cytosine methylation and gene expressions. EUGR changes cytosine methylation at ~500 loci in male rats at 9 weeks of age, preceding the development of PAH and these represent candidate loci for mediating the pathogenesis of pulmonary vascular disease that occurs later in life. These results demonstrate that epigenetic dysregulation is a strong mechanism for propagating the cellular memory of early postnatal events, causing changes in expression of genes and long term susceptibility to PAH, and further providing a new insight into prevention and treatment of EUGR-related PAH. MeDIP together with microarray analysis demonstrated that significant differences in cytosine methylation between EUGR and control rats. Comparison of EUGR(n=3) vs Control (n=3) male rats' pulmonary vascular endothelial cells in 9-week age old rats
2013-07-10 | E-GEOD-48648 | biostudies-arrayexpress
Project description:Age-related macular degeneration (AMD) is the leading cause of irreversible blindness in the elderly population worldwide. Recent studies have demonstrated strong genetic associations between AMD and single nucleotide polymorphisms (SNPs) within genes such as CFH and HTRA1. However, we found monozygotic twins had discordant AMD phenotypes (one with disease, the other without disease), suggesting that an epigenetic mechanism may control the pathogenesis of AMD. We obtained genomic DNA from the twins' peripheral blood mononuclear cells (PBMCs) and subjected it to DNA methylation-chip analysis (MeDIP-chip) that profiled genome-wide DNA methylation patterns on promoters of all genes and microRNAs. Our MeDIP-chip analysis identified 256 genes with hypo-methylated promoters only in the twins with AMD and 744 genes with hyper-methylated promoters only in the twins with AMD. Importantly, the promoter region of IL17RC was associated with hypo-methylated CpG sites only in the twins with AMD but not in the twins without AMD.
2011-03-21 | GSE28032 | GEO
Project description:To increase our understanding of epigenetic patterns associated with aneuploidy we used constitutional trisomy 8 mosaicism as a model, enabling analyses of single cell clones, harboring either trisomy or disomy 8, from the same patient. We profiled gene and miRNA expression as well as genome-wide and promoter specific DNA methylation and hydroxymethylation patterns in trisomic and disomic fibroblasts, using microarrays and methylated DNA immunoprecipitation. comparison of trisomy 8 cells with disomic as well as reference fibroblasts
2012-12-01 | E-GEOD-40317 | biostudies-arrayexpress
Project description:The series was designed to identify the different methylated single CpGs involved in the pathophysiology of ulcerative colitis. A cohort of n=20 monozygotic twins, discordant for ulcerative colitis was selected. Illumina and Nimblegen platforms were used.
2012-09-27 | E-GEOD-27899 | biostudies-arrayexpress