Genome-wide DNA methylation profiling in Atherosclerotic plaques
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA629985 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Genome wide Methylation profiling of DNA extracted from plaques of atherosclerotic plaque samples (n=14) and of controls (n=4). The Illumina Infinium HumanMethylation450 or HumanMethylation850 BeadChip was used representing potentially methylated CpG sites throughout the genome.
2021-08-31 | GSE149759 | GEO
Project description:We report differential DNA methylation results from human femoral atherosclerotic plaques compared to healthy mammary arteries. 5-methylcytosine containing DNA fragments are captured by methylcytosine binding domain - based MethylCapture assay. Captured fragments are sequenced using Illumina paired-end approach and mapped to human genome (hg19). Results. Hypomethylation of chromosomal DNA predominates in atherosclerotic plaques. Chr14q32.2 was identified for the first time as an extensively hypomethylated area in atherosclerosis with highly induced expression of miR127, -136, -410, -431, and -432
2014-12-01 | GSE53575 | GEO
Project description:miRNA expression profiling of human atherosclerotic plaques
| PRJNA976203 | ENA
Project description:To characterize transcriptional and post-transcriptional changes during human atherosclerosis development, we then performed gene expression profiling analysis using data obtained from RNA-seq of 3 different stages of human carotid atherosclerotic plaques.
2026-04-03 | GSE233403 | GEO
Project description:To investigate the expression profiles of miRNA in atherosclerotic plaques, the global features of miRNAs expression of three normal coronary artery tissues sample pools and three sample pools of advanced atherosclerosis plaques of coronary artery were studied using microarray technology,
2015-02-20 | E-MTAB-2460 | biostudies-arrayexpress
Project description:To characterize transcriptional and post-transcriptional changes during human atherosclerosis development, we then performed gene expression profiling analysis using data obtained from RNA-seq of 3 different stages of human carotid atherosclerotic plaques.
2026-04-03 | GSE233402 | GEO
Project description:We compared gene expression profiles between asymptomatic and symptomatic atherosclerotic plaques from the same patient. This was accomplished by analyzing carotid plaques from four patients with bilateral high-grade carotid artery stenoses one being symptomatic (TIA or stroke) and the other asymptomatic.
2006-02-10 | E-MEXP-268 | biostudies-arrayexpress
Project description:In order to identify potential new biomarkers of atherosclerotic plaque composition we performed a large scale analysis of gene expression patterns in human atherosclerotic lesions. Whole genome expression analysis of 101 peripheral plaques identified a robust gene signature (1514 genes) dominated by inflammatory processes, and cholesterol metabolism and storage genes. Specific pathways enriched in this signature included activation of the Toll-like receptor signaling pathway, T-cell activation, cholesterol efflux, oxidative stress response, inflammatory cytokine production, vasoconstriction and lysosomal activity. Analysis of gene expression in plaque micro-dissected material revealed that the signature is strongly up-regulated in macrophage-rich regions and down-regulated in regions with high smooth muscle cell content. A smaller qPCR biomarker panel and inflammatory composite score (ICS) were developed to facilitate clinical translation of discoveries from gene expression profiling. We found that ICS correlates with histological features related to plaque vulnerability. In addition, ICS is able to separate groups of plaques obtained from symptomatic and asymptomatic patients undergoing carotid endarerectomy. In summary, we identified a robust mRNA biomarker panel associated with histo-pathological as well as clinical hallmarks of vulnerable atherosclerotic plaque. This panel may be used as a diagnostic and prognostic tool in clinical setting to evaluate novel anti-atherosclerotic therapies. 290 human peripheral plaques were excised using the FoxHollow silverhawk catheter and stored in RNAlater. RNA was extracted, amplified and hybridized to Affymetrix/Merck custom 1.0 arrays (GPL10687).
2011-09-30 | E-GEOD-24702 | biostudies-arrayexpress
Project description:In order to identify potential new biomarkers of atherosclerotic plaque composition we performed a large scale analysis of gene expression patterns in human atherosclerotic lesions. Whole genome expression analysis of 101 peripheral plaques identified a robust gene signature (1514 genes) dominated by inflammatory processes, and cholesterol metabolism and storage genes. Specific pathways enriched in this signature included activation of the Toll-like receptor signaling pathway, T-cell activation, cholesterol efflux, oxidative stress response, inflammatory cytokine production, vasoconstriction and lysosomal activity. Analysis of gene expression in plaque micro-dissected material revealed that the signature is strongly up-regulated in macrophage-rich regions and down-regulated in regions with high smooth muscle cell content. A smaller qPCR biomarker panel and inflammatory composite score (ICS) were developed to facilitate clinical translation of discoveries from gene expression profiling. We found that ICS correlates with histological features related to plaque vulnerability. In addition, ICS is able to separate groups of plaques obtained from symptomatic and asymptomatic patients undergoing carotid endarerectomy. In summary, we identified a robust mRNA biomarker panel associated with histo-pathological as well as clinical hallmarks of vulnerable atherosclerotic plaque. This panel may be used as a diagnostic and prognostic tool in clinical setting to evaluate novel anti-atherosclerotic therapies. Total RNA from peripheral plaque (n=101) profiled in the Merck/Agilent 44k v1.1 against a reference pool of total RNA from 7 carotid plaques.
2011-09-30 | E-GEOD-23304 | biostudies-arrayexpress
Project description:Macrophages represent a major immune cell population in atherosclerotic plaques and play central role in the progression of this lipid-driven chronic inflammatory disease. Targeting immunometabolism is proposed as a strategy to revert aberrant macrophage activation to improve disease outcome. Here, we show ATP citrate lyase (Acly) to be activated in inflammatory macrophages and human atherosclerotic plaques. We demonstrate that myeloid Acly deficiency induces a stable plaque phenotype characterized by increased collagen deposition and fibrous cap thickness, along with a smaller necrotic core. In-depth functional, lipidomic, and transcriptional characterization indicate deregulated fatty acid and cholesterol biosynthesis and reduced liver X receptor activation within the macrophages in vitro. This results in macrophages that are more prone to undergo apoptosis, whilst maintaining their capacity to phagocytose apoptotic cells. Together, our results indicate that targeting macrophage metabolism improves atherosclerosis outcome and we reveal Acly as a promising therapeutic target to stabilize atherosclerotic plaques.
2021-03-05 | MTBLS2159 | MetaboLights