Molecular classification of failing hearts from coronary and myopathic patients
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE2014 | GEO | 2005/11/24
SECONDARY ACCESSION(S): PRJNA91833
REPOSITORIES: GEO
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Project description:RNA form the heart a goupe of 9 patients with end stage cardiomyopathy (CAD) and 11 patiensts with coronary artery disease (CAD) was hybridized against pooled RNA form 4 normal nonfailing hearts.
2010-06-06 | E-GEOD-2014 | biostudies-arrayexpress
Project description:Rationale: Epicardial adipose tissue (EAT) has been independently associated with non-calcified, high-risk coronary plaques in low-to intermediate risk subjects. Recently, a bidirectional communication was shown between EAT and diseased coronary arteries. In high-risk patients it is unknown whether quantitative measures of EAT can capture, and which molecular players are involved in this mutual interplay. Objective: In a high-risk population, we aimed to determine how the volume of EAT is linked to coronary artery disease (CAD) and to identify potential EAT-deregulated pathways in CAD patients specifically related to coronary artery calcification (CAC). Methods and Results: In a prospective cohort of 574 degenerative severe aortic stenosis patients referred to cardiac surgery, we quantified fat depots by computed tomography (CT) and performed a comparative quantitative proteomics of thoracic fat, including EAT, mediastinal (MAT) and subcutaneous (SAT) adipose tissues. We did not find an independent association of EAT volume with the severity, distribution and complexity of coronary stenosis in invasive coronary angiography. Although, EAT volume was correlated with high CAC, its cardiovascular risk factors-adjusted association was not significant. Taking as reference non-CAD matched-patients and compared to MAT and SAT, EAT proteomic signature of CAD was characterized by up-regulation of pro-calcifying annexins (Annexin A2, ANXA2), fatty acid binding transporters (FABP4) and inflammatory signaling proteins, and by down-regulation of fetuin-A and redox state regulatory enzymes. In EAT, ANXA2 regulation was positively correlated with CAC. EAT gene expression studies confirmed overexpression of ANXA2 and FABP4 in CAD, but no expression of FETUA was detected. Compared with non-CAD, fetuin-A circulating levels were higher in CAD, whereas no fetuin-A pericardial fluid differences were found. Conclusions: In this high-risk cohort, EAT presented an imbalance of pro-calcifying, pro-inflammatory and lipid transporters mediators. These local EAT-mediated regulatory mechanisms were not reflected by the CT volume of EAT alone.
2022-03-04 | PXD008852 | Pride
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
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 the leading cause of mortality worldwide. We aimed to compare expression of miRNA in the affected artery of acute myocardial infarction (ST-elevation myocardial infarction) male patients versus healthy individuals (control). Blood samples were collected during coronary catheterization from proximal culprit coronary arteries aimed for the interventions or from a random artery in control samples. RNA isolated from serum was used for miRNA high throughput sequencing.
2023-04-23 | GSE230165 | GEO
Project description:We developed a coronary plaque sampling approach that could be applied broadly in live patients with coronary artery disease (CAD) to obtain molecular and cellular insights into human coronary atherosclerosis. Our approach combined RNA retrieval directly from balloons used in percutaneous coronary interventions (PCI) and inexpensive, low-input RNA-Seq using SMART-seq. We generated SMART-Seq libraries from coronary samples from 27 patients. Of the 27 patients, 13 were confirmed to have stable CAD (sCAD) and 14 confirmed to have been performed on lesions causing acute coronary syndrome (ACS). We applied CIBERSORTx to analyze the SMART-seq data from each of the 27 samples. We found fibroblasts and fibromyoctes were enriched, while smooth muscle cells were reduced, in samples from ACS compared with sCAD patients. We identified 371 genes as significantly differential expressed (q<0.05) between sCAD and ACS patients.
2023-07-10 | GSE236610 | GEO
Project description:To understand the mechanism of coronary artery aneurysmal dilatation, we identified and compared the expression of circulating miRNAs in three groups of patients. Group 1 enrolled patients with aneurysmal dilatation of coronary arteries (n = 20), Group 2 included patients with angiographically confirmed coronary artery disease (CAD), whereas Group 3 included 20 patients with normal coronary arteries. The miRNAs were isolated from plasma and profiled using PCR arrays miRCURY LNA Serum/Plasma Focus PCR Panels. We demonstrated that the plasma miRNAs levels were significantly different in Group 1 in collation with Group 2 and Group 3 (fold change > 2 and p < 0.05). The comparison of Group 1 with Group 3 identified twenty-one significantly up-regulated and two down-regulated miRNAs in patients with aneurysmal coronary artery dilatation compared to the control groups. Moreover, we identified six up-regulated and two down-regulated miRNAs in patients with CAD compared to the controls. The third comparison revealed four up-regulated and three down-regulated miRNAs in Group 1, when compared to CAD patients. In conclusion, this study demonstrates the specific signature of plasma miRNA, namely up-regulated and down-regulated, in patients with abnormal dilatation of coronary arteries and the comparison between the groups consisting of atherosclerotic and control patients.
2022-03-18 | GSE198885 | GEO
Project description:Gene expression profile in circulating leukocytes identifies patients with coronary artery disease Peter Sinnaeve, Mark Donahue, Peter Grass, Jacky Vonderscher, David Seo, Pascal Goldschmidt, Christopher Granger Department of Medicine, Duke University, Durham, NC, USA, Novartis Institute for Biomedical Research, Cambridge, Boston, MA, USA Introduction Systemic and local inflammation plays a prominent pathogenetic role in atherosclerotic coronary artery disease (CAD), but the relationship of phenotypic changes in circulating leukocytes and extent of CAD remains unclear. We have investigated whether gene expression patterns in circulating leukocytes are associated with presence and extent of CAD. Methods Patients undergoing coronary angiography were selected according to their Duke CAD index (CADi), a validated angiographical measure of the extent of coronary atherosclerosis that correlates with outcome. RNA was extracted from 110 patients with CAD (CADi>23) and from 112 partially matched controls without CAD (CADi=0). Gene expression was assessed using Affymetrix U133A chips. Genes correlating with CAD were identified using Spearman’s rank correlation, and predictive gene expression patterns were identified using a partial least squares (PLS) regression analysis. Results 160 individual genes were found to significantly correlate with CADi (rho>0.2, P<0.0027), although changes in individual gene expression were relatively small (1.2 to 1.5 fold). Using these 160 genes, the PLS multivariate regression resulted in a highly predictive model (r2=0.764, P<0.001). Cross-validation showed that most of the predictive model was carried by only 8 genes (r2=0.752) (table 1). Conclusion Simultaneous expression pattern of 8 genes appears to be highly predictive for CAD. Peripheral leukocyte gene expression pattern could be a novel non-invasive biomarker for CAD and lead to new pathophysiologic insights. parallel group design
2008-10-31 | E-GEOD-12288 | biostudies-arrayexpress
Project description:This study aims at identifying gene expression patterns in the whole blood that could differentiate patients with severe coronary atherosclerosis from subjects without detectable coronary artery disease (CAD), and assess associations of gene expression patterns with plaque features at coronary CT angiography (CCTA). Patients undergoing CCTA for suspected CAD, with no cardiovascular history, were enrolled. Coronary stenosis was quantified and CCTA plaque features were assessed. The whole-blood transcriptome was analyzed by RNA-Sequencing. We detected highly significant differences in the circulating transcriptome between patients with high-degree coronary stenosis (> 70%) at CCTA and subjects with the absence of coronary plaques. Noteworthy, regression analysis revealed expression signatures associated with Leaman score, segment involved score, segment-stenosis score, and plaque volume with density <150 HU at CCTA. This pilot study shows that patients with significant coronary stenosis are characterized by whole blood transcriptome profiles that may discriminate them from patients without CAD. Furthermore, our results suggest that whole blood transcriptional profiles may predict plaque characteristics.
2022-06-29 | GSE202625 | GEO
Project description:To better understand the fundamental molecular mechanisms that contribute to complex human diseases such as coronary artery disease (CAD), we have created a catalog of genetic variants associated with three stages of transcriptional cis-regulation in primary human coronary artery vascular smooth muscle cells. To this end, we used a pooling approach to map quantitative trait locus associations (QTLs) for TCF21 binding (ChIPseq), chromatin accessibility (ATACseq), and chromosomal looping (HiC). We find significant overlap of these QTLs, and several analyses indicate their relationship to smooth muscle specific genes, the binding of smooth muscle transcription factors, and enrichment in CAD-associated loci. These QTLs are extensively validated and allele-specific chromatin looping at the FN1 disease locus is shown to be mediated by activation of the CAD-associated TGFb1 pathway. In sum, these results uncover thousands of loci affecting cis-regulation in a key cell type for CAD, including many that may contribute to CAD risk.
2020-05-07 | GSE141752 | GEO