Stockholm-Tartu Atherosclerosis Reverse Network Engineering Task (STARNET)
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PROVIDER: PRJNA341430 | ENA |
REPOSITORIES: ENA
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Project description:Stockholm-Tartu Atherosclerosis Reverse Network Engineering Task (STARNET)
| PRJNA341431 | ENA
Project description:<p>STARNET is a genetics of RNA expression study of multiple disease-relevant tissues obtained from living patients with cardiovascular disease. Tissue samples are obtained from blood, atherosclerotic-lesion-free internal mammary artery (MAM) and atherosclerotic aortic root (AOR), subcutaneous fat (SF), visceral abdominal fat (VAF), skeletal muscle (SKLM), and liver (LIV) during open thorax surgery of 600 coronary artery disease (CAD) patients. All patients gave written informed consent. The inclusion criterion was eligibility for coronary artery by-pass graft (CABG) surgery. Patients with other severe systemic diseases, such as active systemic inflammatory disease or cancer, were excluded. The primary clinical end points were the SYNTAX score based on the extent of coronary atherosclerosis assessed from preoperative angiograms. The STARNET patients are Caucasians (31% females); 32% had diabetes, 75% had hypertension, and 67% had hyperlipidemia; and 33% had an MI before age 60. By New York Heart Association criteria, 45% were class I, 42% class II, 9% class III, and 1% class IV. </p> <p>TYPES AND RNA SEQUENCING: 566 DNA genotype and 3577 RNA-seq profiles from seven tissues from 600 STARNET CABG patients passed quality control (on average 511 RNA-seq profiles/tissue). DNA was genotyped with the OmniExpress Exome array (Illumina, ~900k SNPs) and imputed to a total of 14,098,063 DNA variant calls (6,245,505 with minor allele frequency >5%). The STARNET subjects mainly overlap with Caucasian of Northern European (Finnish) descent. RNA sequencing was performed using the HighSeq2000 platform, poly-A (LIV, SKLM, VAF, SF and blood) and ribo-zero (AOR, MAM) protocols with 50-100 bp read lengths, single end to 15-30 million read depth. </p>
| phs001203 | dbGaP
Project description:While our understanding of the single-cell gene expression patterns underlying the transformation of vascular cell types during the progression of atherosclerosis is rapidly improving, the clinical and pathophysiological relevance of these changes remain poorly understood. Single cell RNA sequencing (scRNAseq) data generated with SmartSeq2 (~8000 genes/cell) in nearly 19,000 single cells isolated during atherosclerosis progression in mice with human-like plasma lipoproteins and from humans with asymptomatic and symptomatic carotid plaques was clustered into multiple subtypes. For clinical and pathophysiological context, the advanced-stage and symptomatic subtype clusters were integrated with 135 tissue-specific (atherosclerotic aortic wall, mammary artery, liver, skeletal muscle, and visceral and subcutaneous, fat) gene-regulatory networks (GRNs) inferred from 600 coronary artery disease (CAD) patients in the Stockholm-Tartu Atherosclerosis Reverse Network Engineering Task (STARNET) study.Advanced stages of atherosclerosis progression and symptomatic carotid plaques were largely characterized by three smooth-muscle cells (SMC), and three macrophage (MP) subtype clusters with extracellular matrix organization/osteogenic (SMC), and M1-type pro-inflammatory/Trem2-high lipid-associated (MP) phenotypes. Integrative analysis of these 6 clusters with STARNET revealed significant enrichments of three arterial wall GRNs: GRN33 (MP), GRN39 (SMC) and GRN122(MP) with major contributions to CAD heritability and strong associations with clinical scores of coronary atherosclerosis severity (SYNTAX/Duke scores). The presence and pathophysiological relevance of GRN39 was verified in five independent RNAseq datasets obtained from the human coronary and aortic artery, and primary SMCs and by targeting its top-key drivers, FRZB and ALCAM, in cultured human vascular SMCs.By identifying and integrating the most gene-rich single-cell subclusters of atherosclerosis to date with a CAD framework of GRNs, GRN39 was identified and independently validated as being critical for the transformation of contractile SMCs into an osteogenic phenotype promoting advanced-stage, symptomatic atherosclerosis.
2024-03-05 | GSE260656 | GEO
Project description:While our understanding of the single-cell gene expression patterns underlying the transformation of vascular cell types during the progression of atherosclerosis is rapidly improving, the clinical and pathophysiological relevance of these changes remain poorly understood. Single cell RNA sequencing (scRNAseq) data generated with SmartSeq2 (~8000 genes/cell) in nearly 19,000 single cells isolated during atherosclerosis progression in mice with human-like plasma lipoproteins and from humans with asymptomatic and symptomatic carotid plaques was clustered into multiple subtypes. For clinical and pathophysiological context, the advanced-stage and symptomatic subtype clusters were integrated with 135 tissue-specific (atherosclerotic aortic wall, mammary artery, liver, skeletal muscle, and visceral and subcutaneous, fat) gene-regulatory networks (GRNs) inferred from 600 coronary artery disease (CAD) patients in the Stockholm-Tartu Atherosclerosis Reverse Network Engineering Task (STARNET) study.Advanced stages of atherosclerosis progression and symptomatic carotid plaques were largely characterized by three smooth-muscle cells (SMC), and three macrophage (MP) subtype clusters with extracellular matrix organization/osteogenic (SMC), and M1-type pro-inflammatory/Trem2-high lipid-associated (MP) phenotypes. Integrative analysis of these 6 clusters with STARNET revealed significant enrichments of three arterial wall GRNs: GRN33 (MP), GRN39 (SMC) and GRN122(MP) with major contributions to CAD heritability and strong associations with clinical scores of coronary atherosclerosis severity (SYNTAX/Duke scores). The presence and pathophysiological relevance of GRN39 was verified in five independent RNAseq datasets obtained from the human coronary and aortic artery, and primary SMCs and by targeting its top-key drivers, FRZB and ALCAM, in cultured human vascular SMCs.By identifying and integrating the most gene-rich single-cell subclusters of atherosclerosis to date with a CAD framework of GRNs, GRN39 was identified and independently validated as being critical for the transformation of contractile SMCs into an osteogenic phenotype promoting advanced-stage, symptomatic atherosclerosis.
2024-03-05 | GSE260657 | GEO
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2012-07-31 | E-GEOD-38614 | biostudies-arrayexpress
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