Expression data for pharmacogenomics antiplatelet therapy
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE32226 | GEO | 2012/09/15
SECONDARY ACCESSION(S): PRJNA147205
REPOSITORIES: GEO
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Project description:Antiplatelet therapy is the most important treatment to reduce the risk of developing recurrent thrombosis, and to prevent progression to a complete occlusion of coronary arterial disease (CAD) patients after percutaneous coronary intervention Aim of study was to investigate the relationship between response to antiplatelet drugs and global mRNA gene expression in peripheral blood cells (PBC) in patients with coronary arterial disease (CAD) All patients were treated crhonically with acetylsalicylic acid (ASA) (100 mg/day) and clopidogrel (75 mg/day). Blood samples were drown before PCI to evaluate platelet reactivity by VerifyNow® ASA and P2Y12 assays and mRNA expression was measured by Affymetrix GeneChip Human Exon 1.0 ST array.
2012-09-15 | E-GEOD-32226 | biostudies-arrayexpress
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:Coronary artery disease (CAD) is the leading cause of human morbidity and mortality worldwide, underscoring the need to improve diagnostic strategies. Platelets play a major role, not only in the process of acute thrombosis during plaque rupture, but also in the formation of atherosclerosis itself. MicroRNAs are endogenous small non-coding RNAs that control gene expression and are expressed in a tissue and disease-specific manner. Therefore they have been proposed to be useful biomarkers. It remains unknown whether differences in miRNA expression levels in platelets can be found between patients with premature CAD and healthy controls. Methodology/Principal Findings In this case-control study we measured relative expression levels of platelet miRNAs using microarrays from 12 patients with premature CAD and 12 age- and sex-matched healthy controls. Six platelet microRNAs were significantly upregulated (miR340*, miR451, miR454*, miR545:9.1. miR615-5p and miR624*) and one miRNA (miR1280) was significantly downregulated in patients with CAD as compared to healthy controls. To validate these results, we measured the expression levels of these candidate miRNAs by qRT-PCR in platelets of individuals from two independent cohorts; validation cohort I consisted of 40 patients with premature CAD and 40 healthy controls and validation cohort II consisted of 27 patients with artery disease and 40 healthy relatives. MiR340* and miR624* were confirmed to be upregulated in patients with CAD as compared to healthy controls in both validation cohorts. Conclusion/Significance Two miRNAs in platelets are significantly upregulated in patients with CAD as compared to healthy controls. miRNA array analysis of isolated platelets from subjects with premature coronary artery disease compared to healthy control subjects.
2011-09-30 | E-GEOD-28858 | biostudies-arrayexpress
Project description:Tissue samples have been isolated during corornary artery by-pass grafting (CABG)surgery from the atheroscelrotic arterial wall (AAW, aortic root puncture for proxmal ligation of by-pass vessel), non-atherosclertoci arterial wall (NAAW, distal part of mammary artery used a graft for LAD), liver, skeletal muscle (Recturs m), pericardial mediastinal visceral fat) in CAD patients. Carotid lesions samples from 25 validation patients. We used microarrays to measure global gene expression in these tissues to cluster groups of functionally associated genes and then, second step clustering of patients within each cluster to link clusters to patient phenotypes primarily coronary stenosis (CAD) and Intima media thickness (IMT) in carotid stenosis patients. .
2012-08-21 | GSE40231 | GEO
Project description:Percutaneous coronary intervention (PCI) with stent placement is a standard treatment for coronary artery disease (CAD). Despite all medical advances, restenosis remains a challenging clinical problem. However, the molecular and biochemical pathways of restenotic process are not fully understood yet. Furthermore, as restenosis is assumed to be a multigenetic process and genetic predisposition is considered an important risk factor, analysis of the genome-wide gene expression is recommended for better insight of the phenomenon. We used microarray technology to monitor thousands of genes expression simultaneously. The whole genome expression will be analyzed with this technique to identify cluster of up-regulated and down-regulated genes which may be involved in this complex pathological condition. Coronary restenosis after percutaneous coronary intervention remains a challenging problem, despite all medical advances. Molecular and biochemical pathways of restenotic process are not fully understood yet. Furthermore, as restenosis is assumed to be a multigenetic process. We used microarray technology to monitor thousands of genes expression simultaneously in restenosis postive group with reference restenosis negative group, which will unravel potentially modifiable pathways, possible targets and biomarkers for coronary restenosis.
2014-04-30 | E-GEOD-46560 | biostudies-arrayexpress
Project description:An unanticipated complication of the use of bare metal stents in percutaneous transluminal coronary angioplasty is in-stent restenosis resulting in >50% late lumen diameter loss in treated patients. In an effort to reduce in-stent restenosis, drug eluting stents containing the immunosuppressant sirolimus or zotarolimus have recently been developed. We report here the molecular response of arterial tissue to the implanting of these drug-eluting stents.
2011-04-22 | GSE28781 | GEO
Project description:Tissue samples have been isolated during corornary artery by-pass grafting (CABG)surgery from the atheroscelrotic arterial wall (AAW, aortic root puncture for proxmal ligation of by-pass vessel), non-atherosclertoci arterial wall (NAAW, distal part of mammary artery used a graft for LAD), liver, skeletal muscle (Recturs m), pericardial mediastinal visceral fat) in CAD patients. Carotid lesions samples from 25 validation patients. We used microarrays to measure global gene expression in these tissues to cluster groups of functionally associated genes and then, second step clustering of patients within each cluster to link clusters to patient phenotypes primarily coronary stenosis (CAD) and Intima media thickness (IMT) in carotid stenosis patients. . All samples were taken during surgery. The time of operation was less than 3 hours in most instances. Sammon plots show strong clustering of tissue-specific arrays. Even separating AAW from NAAW and carotid lesions.
2012-08-21 | E-GEOD-40231 | biostudies-arrayexpress
Project description:Apolipoprotein C-III was recently acknowledged as a prognostic marker for cardiovascular risk. High levels of Apo-CIII strongly correlate with hypertriglyceridemia and are associated with atherosclerosis and coronary heart disease (CAD). Aim of the present research was to study the plasma proteome profiles of stable CAD patients characterized by different levels of total Apo-CIII. Two subgroups of CAD patients with divergent concentrations (under and upper the median concentration of the population distribution=10mg/dL) of total circulating Apo C-III were examined using a shotgun proteomic approach. 180 plasma proteins of CAD patients were quantified and the data were analyzed by bioinformatic tools and multivariate statistics. The fold change analysis and the Partial Least Square Discriminant Analysis showed a clear separation of the two groups. The dynamic processes that involve Apo C-III concentration in blood and its relation with all other plasma proteins were considered. Lipoproteins (Apo C-II and Apo E), retinol-binding protein 4 and vitronectin were up-regulated in patients with high Apo C-III, while alpha 1-antitrypsin was down-regulated. In this pilot study, the different expression of plasma proteins through the entire range of concentrations of Apo C-III was defined, suggesting possible new players involved in the APO C-III-associated process of arterial damage
2018-07-05 | PXD005973 | Pride
Project description:An unanticipated complication of the use of bare metal stents in percutaneous transluminal coronary angioplasty is in-stent restenosis resulting in >50% late lumen diameter loss in treated patients. In an effort to reduce in-stent restenosis, drug eluting stents containing the immunosuppressant sirolimus or zotarolimus have recently been developed. We report here the molecular response of arterial tissue to the implanting of these drug-eluting stents. Gene expression profiling was performed on 4 artery segments surrounding bare metal stents (BMS), 4 artery segments surrounding sirolimus-eluting stents (SES), and 4 artery segments surrounding zotarolimus-eluting stents (ZES) implanted into porcine animal models for 28 days.
2011-04-22 | E-GEOD-28781 | 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