Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

55 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

A comparison of genome-wide DNA methylation patterns between different tissues from patients with coronary heart disease

ABSTRACT: Using the Illumina Infinium Human Methylation27 BeadChip, we performed a genome-wide analysis of DNA methylation in right coronary artery in the area of advanced atherosclerotic plaques, atherosclerotic-resistant internal mammary arteries, and great saphenous veins obtained from same patients with coronary heart disease. The resulting DNA methylation patterns were markedly different between all the vascular tissues. The genes hypomethylated in athero-prone arteries to compare with atherosclerotic-resistant arteries were predominately involved in regulation of inflammation and immune processes, as well as development. The great saphenous veins exhibited an increase of the DNA methylation age in comparison to the internal mammary arteries. Gene ontology analysis for genes harboring hypermethylated CpG-sites in veins revealed the enrichment for biological processes associated with the development. Four CpG-sites located within the MIR10B gene sequence and about 1 Kb upstream of the HOXD4 gene were also confirmed as hypomethylated in the independent dataset of right coronary arteries in the area of advanced atherosclerotic plaques in comparison with the other vascular tissues. Bisulfite converted genomic DNA from 24 samples was denatured, whole-genome amplified, fragmented and subsequently hybridized to the Illumina Infinium 27k Human Methylation Beadchip.

ORGANISM(S): Homo sapiens

SUBMITTER: Anton Markov

PROVIDER: E-GEOD-62867 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Epigenome analysis of normal and preeclamptic placenta samples

Project description:Preeclampsia (PE), a hypertensive disorder of pregnancy, is hypothesized to be associated with, if not mechanistically related to abnormal placental function. However, the exact mechanisms regulating the pathogenesis of PE remain unclear. While many studies have investigated changes in gene expression in the PE placenta, the role of epigenetics in PE associated placental dysfunction remains unclear. Using the genome-wide Illumina Infinium Methylation 450 BeadChip array, we analyzed gene-specific alterations in DNA methylation in placental biopsies collected from normal pregnant women delivering at term (n=14), with term PE (≥37 weeks; n=19) or with preterm PE (<37 weeks, n=12). Of the 485,582 gene loci on the array, compared to controls, 229 loci were differentially methylated in PE placentas and 3411 loci were differentially methylated in preterm PE (step up p-value <0.05 and >5% methylation difference). Functional annotation of the differentially methylated genes in preterm PE placentas revealed a 32 gene cluster in the cadherin and cell adhesion functional groups (Benjamini p<0.00001). Hypermethylation of CDH11 (p=0.0143), COL5A1 (p=0.0127) and TNF (p=0.0098) and hypomethylation of NCAM1 (p=0.0158) was associated with altered mRNA expression in preterm PE placentas. These studies demonstrate aberrant methylation, correlating with disease severity, in PE placentas. Bisulphite converted DNA from the 45 samples were hybridised to the Illumina Infinium 450k Human Methylation Beadchip v1.2

2014-05-20 | E-GEOD-57767 | biostudies-arrayexpress

Methylation profiles of esophageal squamous cell carcinoma patients and cancer-free individual in Taiwan.

Project description:Genome wide DNA methylation profiling of tumor and normal samples with esophageal squamous cell carcinoma patients. The Illumina GolodenGate methylation cancer panel I was used to obtain DNA methylation profiles across approximately 1,505 CpGs in esophageal squemous cell carcinoma samples. Samples included normal, tumors and plasma samples with esophageal squamous cell carcinoma, also inculding the plasma samples with cancer-free individual. Bisulfite converted DNA from the 288 samples were hybridised to the Illumina GolodenGate methylation cancer panel I

2014-09-11 | E-GEOD-51287 | biostudies-arrayexpress

Gene Body Methylation Directly Increases Gene Expression and is a Therapeutic Target for Genes Upregulated in Cancer

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-08-01 | E-GEOD-51815 | biostudies-arrayexpress

An Inhibitor of Mutant IDH1 Delays Growth and Promotes Differentiation of Glioma Cells Methylation Data for Xenograft Samples

Project description:The recent discovery of mutations in metabolic enzymes has rekindled interest in harnessing the altered metabolism of cancer cells for cancer therapy. One potential drug target is isocitrate dehydrogenase 1 (IDH1) which is mutated in multiple human cancers. Here, we examine the role of mutant IDH1 in fully transformed cells with endogenous IDH1 mutations. A selective R132H-IDH1 inhibitor (AGI-5198) identified through a high-throughput screen dose-dependently blocked the ability of the mutant enzyme (mIDH1) to produce R-2-hydroxyglutarate (R-2HG). Under conditions of near complete R-2HG inhibition, the mIDH1 inhibitor induced demethylation of histone H3K9M3 and expression of genes associated with gliogenic differentiation. Blockade of mIDH1 impaired the growth of IDH1-mutant - but not IDH1-wildtype – glioma cells without appreciable changes in genome wide DNA methylation. These data suggest that mIDH1 may promote glioma growth through mechanisms beyond its well-characterized epigenetic effects. Xenograft experiments were carried out with treatment cohorts of vehicle, 150mg/kg/day, 450mg/kg/day. After the indicated tumors were harvested and genomic DNA was extracted and analyzed by the Illumina 450k Methylation array.

2013-04-04 | E-GEOD-45198 | biostudies-arrayexpress

An Inhibitor of Mutant IDH1 Delays Growth and Promotes Differentiation of Glioma Cells

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-04-04 | E-GEOD-45200 | biostudies-arrayexpress

An Inhibitor of Mutant IDH1 Delays Growth and Promotes Differentiation of Glioma Cells Methylation Data for In Vitro Model

Project description:The recent discovery of mutations in metabolic enzymes has rekindled interest in harnessing the altered metabolism of cancer cells for cancer therapy. One potential drug target is isocitrate dehydrogenase 1 (IDH1) which is mutated in multiple human cancers. Here, we examine the role of mutant IDH1 in fully transformed cells with endogenous IDH1 mutations. A selective R132H-IDH1 inhibitor (AGI-5198) identified through a high-throughput screen dose-dependently blocked the ability of the mutant enzyme (mIDH1) to produce R-2-hydroxyglutarate (R-2HG). Under conditions of near complete R-2HG inhibition, the mIDH1 inhibitor induced demethylation of histone H3K9M3 and expression of genes associated with gliogenic differentiation. Blockade of mIDH1 impaired the growth of IDH1-mutant - but not IDH1-wildtype – glioma cells without appreciable changes in genome wide DNA methylation. These data suggest that mIDH1 may promote glioma growth through mechanisms beyond its well-characterized epigenetic effects. Samples were maintained in either DMSO or 1.5uM 5198 for 2 passages up to 20 passages. Biological replicates for each passage and treatment was collected and genomic DNA was extracted and analyzed on the Illumina 450K Methylation platform for a total of 16 samples.

2013-04-04 | E-GEOD-45199 | biostudies-arrayexpress

Low dose of DNA-demethylating agents target colorectal cancer-initiating cells by activation of RIG1/MAVS signaling pathway

Project description:Genome wide DNA methylation profiling of 3 patient-derived colorectal cancer samples with different CIMP profiles. The Illumina Infinium 450k Human DNA methylation Beadchip was used to obtain DNA methylation profiles across approximately 450,000 CpGs Bisulphite converted DNA from the 3 samples were hybridised to the Illumina HumanMethylation450 BeadChip

2015-08-27 | E-GEOD-62086 | biostudies-arrayexpress

Epigenome analysis of irradiated and non-irradiated breast tumor tissue samples and normal controls

Project description:Genome wide DNA methylation profiling of irradiated and non-irradiated breast tumor samples and normal control tissue. The Illumina Infinium 27k Human DNA methylation Beadchip, Genome Build 36 was used to obtain DNA methylation profiles across approximately 27,000 CpGs in breast tumor samples. Samples included 20 non-irradiated tumor samples, 19 irradiated tumor samples and 9 normal controls. Bisulphite converted DNA from the 48 samples were hybridised to the Illumina Infinium 27k Human Methylation Beadchip v1.2

2014-03-26 | E-GEOD-50220 | biostudies-arrayexpress

Codeletion of 1p and 19q Determines Distinct Gene Methylation and Expression Profiles in IDH-mutated Oligodendroglial Tumors

Project description:Genome wide DNA methylation profiling of oligodendroglial tumors (OTs) and five non tumoral brain tissue (NTBT) samples. The Illumina Infinium Human DNA methylation 450k Beadchip was used to obtain DNA methylation profiles across approximately 450,000 CpGs in tumoral samples. Samples included 46 OTs and 5 NTBT. Bisulphite converted DNA from the 51 samples were hybridised to the Illumina Infinium 450k Human Methylation Beadchip

2014-09-06 | E-GEOD-61160 | biostudies-arrayexpress

Aberrant DNA methylation profiling of classic Philadelphia Negative Myeloproliferative Neoplasms

Project description:Since most DNA methylation studies in Classic Philadelphia-negative myeloproliferative neoplasms (MPNs) M-bM-^@M-^S polycythaemia vera (PV), essential thrombocythaemia (ET), and primary myelofibrosis (PMF) - have been performed on a gene-by-gene basis, a more comprehensive methylation profiling is needed to know the real implication of this alteration. In order to investigate the DNA methylation profile in chronic and transformed phase MPNs, we performed genome-wide DNA methylation arrays in 71 chronic (24 PV, 23 ET and 24 PMF) and 13 transformed MPNs. The three types of chronic MPNs showed the same aberrant DNA methylation pattern when compared to controls. Differentially methylated genes (DMG) were enriched in a gene network centered on the NF-M-NM-:B pathway, indicating that they may be involved in the pathogenesis of these diseases. In the case of transformed MPNs we detected an increased number of DMGs with respect to chronic MPNs. Interestingly, these genes were enriched in a list of DMGs in primary AMLs and in a gene network centered around the IFN pathway. Further studies are clearly needed to elucidate the role of DMGs in MPNs, but our results suggest that this alteration plays an important role in the pathogenesis and transformation of MPNs and that modulation of these pathways would allow us to improve the quality of life of these patients. The methylation profile of 24 PBMCs samples from patients diagnosed with Policytemia Vera, 23 from Essential Thrombocythemia and 24 from primary myelofibrosis was assessed. We also included 13 secondary acute myeloid leukaemia (AML): 5 transformed PMF,4 transformed TE and 4 transformed PV. As reference,4 healthy donor PBMCs samples from whole peripheral blood and 4 PBMCs samples from bone marrow were used.

2013-11-29 | E-GEOD-42042 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data