Homo sapiens
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PROVIDER: PRJNA357933 | ENA |
REPOSITORIES: ENA
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Project description:Center for Common Disease Genomics [CCDG] – Cardiovascular: VIRGO: Variation in Recovery - Role of Gender on Outcomes of Young Acute Myocardial Infarction (AMI) Patients
| PRJNA357932 | ENA
Project description:Whole-genome gene expression analysis has been successfully utilized to diagnose, prognosticate, and identify potential therapeutic targets for cardiovascular disease. However, the utility of this approach to identify outcome-related genes and dysregulated pathways following first-time myocardial infarction (AMI) remains unknown and may offer a novel strategy to detect affected expressome networks that predict long-term outcome. Whole-genome microarray and targeted cytokine expression profiling on blood samples from normal cardiac function controls and first-time AMI patients within 48-hours post-MI revealed expected differential gene expression profiles enriched for inflammation and immune-response pathways in AMI patients. To determine molecular signatures at the time of AMI that could prognosticate long-term outcomes, transcriptional profiles from sub-groups of AMI patients with (n=5) or without (n=22) any recurrent events over an 18-month follow-up were compared. This analysis identified 559 differentially expressed genes. Bioinformatic analysis of this differential gene set for associated pathways revealed 1) increasing disease severity in AMI patients is associated with a decreased expression of the developmental epithelial-to-mesenchymal transition, and 2) modulation of cholesterol transport genes that include ABCA1, CETP, APOA1, and LDLR is associated with clinical outcome. In conclusion, differentially regulated genes and modulated pathways were identified that predicted recurrent cardiovascular outcomes in first-time AMI patients. This cell-based approach for risk stratification in AMI warrants a larger study to determine the role of metabolic remodeling and regenerative processes required for optimal outcomes. A validated transcriptome assay could represent a novel, non-invasive platform to anticipate modifiable pathways and therapeutic targets to optimize long-term outcome for AMI patients. The overall experimental design includes blood samples from 21 control and 31 myocardial infaction patient groups. Among the 31patients, 5 patients have recurrent events. Microarray were peformed on the blood samples and comparisons of control vs patient and patients with recurrent events vs patients without recurrent events were performed to identify differential genes related to disease or patients groups with recurrent events for the following bioinformatic analysis.
2014-02-28 | E-GEOD-48060 | biostudies-arrayexpress
Project description:MicroRNAs are important cellular components and their dysfunctions are associated with various disease. Acute myocardial infarction (AMI) is one of the most serious cardiovascular diseases. Although several miRNAs have been reported to be associated with AMI, more novel miRNAs are needed to be investigated to ascertain if they are associated with AMI.
2010-01-05 | GSE19695 | GEO
Project description:Despite the significant reduction in the overall burden of cardiovascular disease (CVD) over the past decade, CVD still accounts for a third of all deaths in the United States and worldwide each year. While efforts to identify and reduce risk factors for atherosclerotic heart disease (i.e. hypertension, dyslipidemia, diabetes mellitus, cigarette smoking, inactivity) remain the focus of primary prevention, the inability to accurately and temporally predict acute myocardial infarction (AMI) impairs our ability to further improve patient outcomes. Our diagnostic evaluation for the presence of coronary artery disease relies on functional testing, which detects flow-limiting coronary stenosis, but we have known for decades that most lesions underlying AMI are only of mild to moderate luminal narrowings, not obstructing coronary blood flow. Accordingly, there is a dire need of improved diagnostics for underlying arterial plaque dynamics, fissure and rupture. Here we describe the designation of a specific gene expression pattern acting as a molecular signature for acute myocardial infarction present in whole blood of patients that was determined using microarray analysis of enriched circulating endothelial cells (CEC). We isolated circulating endothelial cells from patients experience acute myocardial infartion and healthy cohorts, and measured gene expression using the HG-133U_PLUS_2 microarray Circulating endothelial cells were isolated from patients experiencing acute myocardial infarction (n=49) and from healthy cohorts (n=50). The patients were separated into a discovery cohort (n=43) for biomarker discovery and model training; and into a validation cohort (n=56) for biomarker validation and model testing.
2015-02-28 | E-GEOD-66360 | biostudies-arrayexpress
Project description:MicroRNAs are important cellular components and their dysfunctions are associated with various disease. Acute myocardial infarction (AMI) is one of the most serious cardiovascular diseases. Although several miRNAs have been reported to be associated with AMI, more novel miRNAs are needed to be investigated to ascertain if they are associated with AMI. SD rats (180-200g) was divided into sham-control group and two days group after AMI, seven days group after AMI, fourteen days group after AMI, each group has six individual animals total RNA was taken from the border-zone myocardium , low molecular weight RNA was seperate and labeled , and then hybridized to capitalbio V2 biochip representing about 924 microRNA . three chip were test in each group, and the procedure was repeated twice.
2010-04-22 | E-GEOD-19695 | biostudies-arrayexpress
Project description:The recovery from acute myocardial infarction (AMI) is influenced by physiological and psychological factors. While the physiological effects have been extensively studied, the contribution of psychological factors and whether they can be modulated is not completely clear. Here we show that the activity of the reward system, a brain network involved in motivation and positive expectation, affects outcomes in mice following AMI. We found that chemogenetic activation of dopaminergic neurons in the ventral tegmental area (VTA) significantly attenuated the remodeling process following AMI, resulting in improved left-ventricular performance compared to controls. VTA activation was associated with modulation of the immune response following AMI and increased blood vessel formation in the damaged area, mediated, at least in part, by changes in liver-secreted proteins. Together, our findings reveal a potential mechanism by which specific brain activity can affect the multifactorial systemic and local tissue response to AMI, introducing a novel target for therapeutic interventions
2024-05-03 | PXD043448 | Pride
Project description:Background: Aortic valve sclerosis (AVSc) presents similar pathogenetic mechanisms to coronary artery disease (CAD) and is associated with both short- and long-term mortality. In the context of acute myocardial infarction (AMI), evidence of specific systemic mechanisms characterizing AVSc are currently lacking. Objective: To evaluate the systemic pathophysiological landscape that might differentiate AVSc from non-AVSc subjects in AMI. Methods: Whole-blood transcriptome of AVSc (n=44) and no-AVSc (n=66) patients with AMI was assessed by RNA-sequencing. A bioinformatic workflow, including feature selection, differential expression and enrichment analysis was performed to identify gene expression signatures discriminating AVSc from no-AVSc and infer functional association. Multivariable Cox regression analysis was used to estimate hazard ratio of AVSc versus no-AVSc patients. Results: A signature of 100 informative genes allowed classifying AVSc from no-AVSc with 94% accuracy. Significant differences in 143 genes were also identified, 30 of which withstood association independently of age and previous AMI, or cardiac interventions. Functional inference unveiled significant association of AVSc with acute inflammatory and type I interferons (IFNs) response, platelet activation and hemostasis. AMI patients with AVSc showed a significantly higher incidence of adverse cardiovascular events within 10 years of follow-up with a full adjusted hazard ratio of 2.4 (95% CI 1.3–4.5). Conclusions: During AMI, AVSc patients showed increased type I IFNs response and associated adverse cardiovascular outcomes at follow-up. Novel pharmacological therapies aiming to inhibit response to type I IFNs during or immediately after AMI might improve poor cardiovascular outcomes of AMI patients with AVSc.
2024-01-31 | GSE218474 | GEO
Project description:Whole-genome gene expression analysis has been successfully utilized to diagnose, prognosticate, and identify potential therapeutic targets for cardiovascular disease. However, the utility of this approach to identify outcome-related genes and dysregulated pathways following first-time myocardial infarction (AMI) remains unknown and may offer a novel strategy to detect affected expressome networks that predict long-term outcome. Whole-genome microarray and targeted cytokine expression profiling on blood samples from normal cardiac function controls and first-time AMI patients within 48-hours post-MI revealed expected differential gene expression profiles enriched for inflammation and immune-response pathways in AMI patients. To determine molecular signatures at the time of AMI that could prognosticate long-term outcomes, transcriptional profiles from sub-groups of AMI patients with (n=5) or without (n=22) any recurrent events over an 18-month follow-up were compared. This analysis identified 559 differentially expressed genes. Bioinformatic analysis of this differential gene set for associated pathways revealed 1) increasing disease severity in AMI patients is associated with a decreased expression of the developmental epithelial-to-mesenchymal transition, and 2) modulation of cholesterol transport genes that include ABCA1, CETP, APOA1, and LDLR is associated with clinical outcome. In conclusion, differentially regulated genes and modulated pathways were identified that predicted recurrent cardiovascular outcomes in first-time AMI patients. This cell-based approach for risk stratification in AMI warrants a larger study to determine the role of metabolic remodeling and regenerative processes required for optimal outcomes. A validated transcriptome assay could represent a novel, non-invasive platform to anticipate modifiable pathways and therapeutic targets to optimize long-term outcome for AMI patients.
2014-02-28 | GSE48060 | GEO
Project description:Analysis of peripheral blood specimens from patients with acute myocardial infarction (AMI). Results provide insight into molecular mechanisms associated with AMI.
2018-12-08 | GSE123487 | GEO
Project description:Despite the significant reduction in the overall burden of cardiovascular disease (CVD) over the past decade, CVD still accounts for a third of all deaths in the United States and worldwide each year. While efforts to identify and reduce risk factors for atherosclerotic heart disease (i.e. hypertension, dyslipidemia, diabetes mellitus, cigarette smoking, inactivity) remain the focus of primary prevention, the inability to accurately and temporally predict acute myocardial infarction (AMI) impairs our ability to further improve patient outcomes. Our diagnostic evaluation for the presence of coronary artery disease relies on functional testing, which detects flow-limiting coronary stenosis, but we have known for decades that most lesions underlying AMI are only of mild to moderate luminal narrowings, not obstructing coronary blood flow. Accordingly, there is a dire need of improved diagnostics for underlying arterial plaque dynamics, fissure and rupture. Here we describe the designation of a specific gene expression pattern acting as a molecular signature for acute myocardial infarction present in whole blood of patients that was determined using microarray analysis of enriched circulating endothelial cells (CEC). We isolated circulating endothelial cells from patients experience acute myocardial infartion and healthy cohorts, and measured gene expression using the HG-133U_PLUS_2 microarray
2015-02-28 | GSE66360 | GEO