Expression profiles of human carotid plaques
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE12828 | GEO | 2008/09/19
SECONDARY ACCESSION(S): PRJNA111135
REPOSITORIES: GEO
Similar Datasets
Project description:This analysis compares gene expression in human carotid plaques with gene expression in major tissues and cell types in the human body (GSE1133, Su et al. 2004). Experiment Overall Design: Human carotid endarterectomies were isolated from six subjects with symptomatic carotid artery disease.
2008-10-25 | E-GEOD-12828 | biostudies-arrayexpress
Project description:A microarray analysis of advanced human atherosclerotic carotid artery plaques (equal or over 70% stenosis, NASCET criteria) from radiologically confirmed ipsilateral stroke patients (stroke-susceptible plaques, n=12) compared with carotid plaques collected from clinically asymptomatic patients with clear brain imaging (asymptomatic plaques, n=9) with equivalent conventional risk factors and severity of carotid stenosis.
2011-12-30 | E-MEXP-2257 | biostudies-arrayexpress
Project description:Single Cell Transcriptomics of human carotid artery plaques
| PRJNA1036676 | ENA
Project description:Atherosclerotic plaque rupture is the etiology of ischemic stroke and myocardial infarction. Ribosome-depleted total RNA was sequenced from carotid plaques obtained from patients undergoing carotid endarterectomy with high-grade stenosis and either 1) a carotid-related ischemic cerebrovascular event within the previous 5 days ('recently ruptured,' n=6) or 2) an absence of a cerebrovascular event ('asymptomatic,' n=5). Examination of the differentially expressed genes supported the importance of inflammation and inhibition of proliferation and migration coupled with an increase in apoptosis. Thus, the transcriptome of recently ruptured plaques is enriched with transcripts associated with inflammation and fibrous cap thinning and support further examination of the role of B lymphocytes and interferons in atherosclerotic plaque rupture.
2022-08-10 | GSE198600 | GEO
Project description: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.
2015-05-14 | GSE66500 | GEO
Project description:Protein profiles were determined from different distinct regions of human atherosclerotic plaques, including: internal control, fatty streak, plaque shoulder, plaque centre, and fibrous cap. Protein extracts from all 5 regions, from 3 men and 3 women, were separated by two-dimensional gel electrophoresis (in total 30 2-DE gels). Stained gels were matched by protein spot distribution, and a protein mapping was performed to identify as many protein spots as possible, by MALDI-TOF MS / peptide mass fingerprinting (Voyager DE Pro; Applied Biosystems). This resulted in the identification of 97 protein spots, corresponding to 52 unique protein by accession number. To expand on this nLC-MS/MS (Easy-nLC / LTQ Orbitrap Velos Pro; Thermo Fisher Scientific) experiments were run on additional carotid plaque samples from 10 men and 10 women, using three of the predefined regions; internal control, fatty streak, plaque core. MS/MS analysis resulted in the identification of over 1000 proteins. Human carotid atherosclerotic plaques (n = 26) were obtained from the Linköping Carotid Study, and all methods/protocols described herein have been approved by the local ethics committee (Linköping University Hospital, Linköping, Sweden). Written informed consent was also obtained from all patients.
2016-05-24 | PXD003930 | Pride
Project description:RNA expression data from calcified human carotid atherosclerotic plaques
| PRJNA517476 | ENA
Project description: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. 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.
2015-05-14 | E-GEOD-66500 | biostudies-arrayexpress
Project description:Although unstable atherosclerosis in the carotid bifurcation is a significant etiology behind ischemic stroke, clinical imaging methods to distinguish stable from vulnerable lesions are lacking and selection of patients for stroke-preventive intervention still relies on surrogate variables with moderate predictive power, such as the degree of luminal narrowing. Here we combined clinical and diagnostic imaging information by comuted tomography to select patients with calcified plaques for large scale molecular analysis, in an effort to increase our understanding of the pathophysiology behind carotid plaque instability as related to patient- and plaque- phenotype.
2019-06-01 | GSE125771 | GEO
Project description:Next Generation Sequencing of Asymptomatic and Symptomatic Carotid Atherosclerotic Plaques
| PRJNA816103 | ENA