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Series GSE66500 Query DataSets for GSE66500
Status Public on May 14, 2015
Title DNA methylation dynamics in human carotid plaques after cerebrovascular events
Organism Homo sapiens
Experiment type Methylation profiling by genome tiling array
Summary One pending issue in cardiovascular epigenetics is whether cerebrovascular events, a major complication of atherosclerosis, are associated with any specific DNA methylation changes in the carotid plaque. To clarify that topic, we profiled the DNA methylomes of human symptomatic carotid plaques (SCPs) obtained from patients who suffered cerebrovascular events (n=19) and asymptomatic counterparts (ACP; n=19) with a high-density microarray (~485,000 CpG sites, Illumina), and crossed DNA methylation data with RNAseq-based expression data from an independent SCP set (n=8). Few (30) CpGs showed a significant (p<0.05; absolute Delta-Beta>0.20) differential methylation between the two groups. Within SCPs, methylation correlated significantly with post-cerebrovascular event time (PCET; range: 3-45 days; r-value range -0.926 to 0.857; p<0.05) for ~45,000 CpGs, the vast majority of which became hypomethylated with increasing PCET. Hypomethylation was not due to erasure of the gene-body and CG-poor region hypermethylation that accompany the progression of stable lesions, but rather targeted promoters and CpG islands. Noticeably, promoter hypomethylation and increased expression were observed for genes involved in the inhibition of the inflammatory response, defence against oxidative stress and active DNA demethylation. Our data show that only weak changes in the DNA methylome distinguish symptomatic from asymptomatic carotid plaques, but a widespread demethylation resulting in permissive transcriptional marks at atheroprotective gene promoters is established in plaques after a cerebrovascular event, thus mirroring previous observations that ruptured plaques tend to revert to a more stable structure. The identified loci are candidate targets to accelerate the pace of carotid plaque stabilization.
Overall design DNA was quantified by Quant-iT PicoGreen dsDNA Reagent (Invitrogen) and the integrity was analyzed in a 1.3% agarose gel. Bisulfite conversion of 600 ng of each sample was perform according to the manufacturer's recommendation for Illumina Infinium Assay. Effective bisulphite conversion was checked for three controls that were converted simultaneously with the samples. 4 ul of bisulfite converted DNA were used to hybridize on Infinium HumanMethylation 450 BeadChip, following Illumina Infinium HD Methylation protocol. Chip analysis was performed using Illumina HiScan SQ fluorescent scanner. The intensities of the images are extracted using GenomeStudio (2011.2) Methylation module (1.8.5) software. Methylation score of each CpG is represented as beta value.
Contributor(s) Zaina S, Moran S, Esteller M
Citation(s) 26088578
Submission date Mar 04, 2015
Last update date Mar 22, 2019
Contact name Sebastian Moran
Organization name IDIBELL
Department PEBC
Street address Av. Gran Via de l'Hospitalet, 199-203
City L'Hospitalet del Llobregat
State/province Barcelona
ZIP/Postal code 08908
Country Spain
Platforms (1)
GPL13534 Illumina HumanMethylation450 BeadChip (HumanMethylation450_15017482)
Samples (38)
GSM1624132 30-Asymptomatic
GSM1624133 154-Asymptomatic
GSM1624134 172-Asymptomatic
BioProject PRJNA277167

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SOFT formatted family file(s) SOFTHelp
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Series Matrix File(s) TXTHelp

Supplementary file Size Download File type/resource
GSE66500_RAW.tar 183.1 Mb (http)(custom) TAR
GSE66500_ResultsMatrix.txt.gz 248.3 Mb (ftp)(http) TXT
Processed data included within Sample table
Processed data are available on Series record

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