Genetic variants associated with coronary artery disease in Indians
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA429566 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Genetic variations were successfully associated among patients with coronary artery disease using Illumina Cardiometabochip containing 1,96,725 SNPs Illumina Cardio-metabochip is a custom designed SNP microarray containing 1,96,725 SNPs designed by several GWAS and consortia
2021-01-11 | GSE109068 | GEO
Project description:Global gene expression profile of whole blood in patients with coronary artery disease (CAD) showed significant upregulation of 343 genes and down regulation of 151 genes as compared to controls (p<0.05). There was predominant differential regulation of inflammatory and immune response genes as well as early growth response genes in our dataset. Of the ten candidate genes selected for validation by real time PCR in an independent cohort, CXCL1, EGR3, IL8, PTGS2 and CD69 genes were up regulated and IFNG and FASLG down regulated in cases relative to controls. We selected 13 patients with angiographically confirmed coronary artery disease (CAD) between ages 40 - 55 years and 11 population-based asymptomatic controls with normal ECG and matched for age, gendre and common risk factors such as diabetes and hypertension to that of the cases. Global gene expression profiling was performed on the Agilent microarray platform.
2012-11-09 | E-GEOD-42148 | biostudies-arrayexpress
Project description:The human LncRNA microarray analysis of the 6 monocytes samples from Coronary Artery Disease patients and non Coronary Artery Disease 3 Coronary Artery Disease patients and 3 non-Coronary Artery Disease donors
2015-06-05 | E-GEOD-69587 | biostudies-arrayexpress
Project description:Coronary artery disease (CAD) is the leading cause of mortality and morbidity driven by both genetic and environmental risk factors. Meta-analyses of genome-wide association studies (GWAS) have identified multiple single nucleotide polymorphisms (SNPs) associated with CAD and myocardial infarction (MI) susceptibility in multi-ethnic populations. The majority of these variants reside in non-coding regulatory regions and are co-inherited with hundreds of candidate regulatory SNPs. Herein, we use integrative genomic, epigenomic, and transcriptomic fine-mapping in human coronary artery smooth muscle cells (HCASMC) and tissues to identify causal regulatory variation and mechanisms responsible for CAD associations. Using these genome-wide maps we prioritize 65 candidate variants and perform allele-specific binding and expression analyses on 7 top candidates. We validate our findings in two independent cohorts of diseased human arterial expression quantitative trait loci (eQTL), which together demonstrate fundamental links between CAD associations and regulatory function in the appropriate disease context. We performed ATAC-seq, ChIP-seq, and RNA-seq on human coronary artery smooth muscle cells grown in SmGM-2 Smooth Muscle Growth Medium-2 including hEGF, insulin, hFGF-B and FBS, but without antibiotics (Lonza, #CC-3182). For ATAC-seq and RNA-seq we performed stimulations with growth factors (TGF-B1, PDGF-BB, PDGF-DD) versus serum-free control. We conducted two biological replicates for each condition using independent donors. For ATAC-seq experiments, sequencing was completed on an Illumina Hiseq 2500, paired-end 50bp reads. For ChIP-seq we performed immunoprecipitations using H3K27ac (Abcam ab4729). We conducted two biological replicates using HCASMC from independent donors, and also did an IgG control for these studies. For RNA-seq we also conducted two replicates using HCASMC from independent donors. For both ChIP-seq and RNA-seq experiments, sequencing was completed on an Illumina HiSeq 2500, paired-end 100bp reads. We also performed ex-vivo ATAC-seq on frozen tissues (isolated media) from normal and atherosclerotic human coronary arteries, using three independent donors for each. Sequencing was also completed on an Illumina HiSeq 2500, paired end 50bp reads.
2016-07-06 | E-GEOD-72696 | biostudies-arrayexpress
Project description:Coronary artery disease (CAD) is the leading cause of mortality and morbidity driven by both genetic and environmental risk factors. Meta-analyses of genome-wide association studies (GWAS) have identified multiple single nucleotide polymorphisms (SNPs) associated with CAD and myocardial infarction (MI) susceptibility in multi-ethnic populations. The majority of these variants reside in non-coding regulatory regions and are co-inherited with hundreds of candidate regulatory SNPs. Herein, we use integrative genomic, epigenomic, and transcriptomic fine-mapping in human coronary artery smooth muscle cells (HCASMC) and tissues to identify causal regulatory variation and mechanisms responsible for CAD associations. Using these genome-wide maps we prioritize 65 candidate variants and perform allele-specific binding and expression analyses on 7 top candidates. We validate our findings in two independent cohorts of diseased human arterial expression quantitative trait loci (eQTL), which together demonstrate fundamental links between CAD associations and regulatory function in the appropriate disease context.
2016-07-06 | GSE72696 | GEO
Project description:Global gene expression profile of whole blood in patients with coronary artery disease (CAD) showed significant upregulation of 343 genes and down regulation of 151 genes as compared to controls (p<0.05). There was predominant differential regulation of inflammatory and immune response genes as well as early growth response genes in our dataset. Of the ten candidate genes selected for validation by real time PCR in an independent cohort, CXCL1, EGR3, IL8, PTGS2 and CD69 genes were up regulated and IFNG and FASLG down regulated in cases relative to controls.
2012-11-09 | GSE42148 | GEO
Project description:The human LncRNA microarray analysis of the 6 monocytes samples from Coronary Artery Disease patients and non Coronary Artery Disease
2015-06-05 | GSE69587 | GEO
Project description:The human LncRNA microarray analysis of the 6 plasma samples from Coronary Artery Disease patients and non Coronary Artery Disease
2015-05-05 | GSE68506 | GEO
Project description:Genome-wide association studies (GWAS) have identified hundreds of genetic risk loci for coronary artery disease (CAD). However, non-European populations are underrepresented in coronary artery disease (CAD). However, non-European populations are underrepresented in GWAS and the causal gene-regulatory mechanisms of these risk loci during atherosclerosis remain unclear. We incorporated local ancestry and haplotype information to identify quantitative trait loci (QTL) for gene expression and splicing in coronary arteries obtained from 138 ancestrally diverse Americans.
2023-11-14 | GSE225650 | GEO
Project description:Coronary artery disease (CAD) is a complex inflammatory disease of the vessel wall and often leads to myocardial infarction. Genome-wide association studies (GWAS) have now identified over 200 genetic loci associated with CAD. The majority of CAD-associated variants are located in noncoding regions of the genome, many of which are predicted to regulate chromatin accessibility and gene expression. In this study, we performed ATAC-seq in human coronary artery patient samples to identify novel chromatin accessibility QTLs (caQTLs) and gain additional insights into CAD regulatory mechanisms in vivo.
2022-01-24 | GSE188422 | GEO