Characterisation of Myocardial Infarction and Unstable Angina with mRNA Profiles from Whole Blood of individual patients
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE29111 | GEO | 2011/05/06
SECONDARY ACCESSION(S): PRJNA140377
REPOSITORIES: GEO
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Project description:Coronary artery disease (CAD) remains a leading cause of death worldwide. Acute coronary syndromes (ACS) are the spectrum of diseases arising from coronary atherosclerotic plaque rupture, ranging from unstable angina (UA; clinical symptoms of cardiac ischemia without myocardial necrosis) to myocardial infarction (MI; clinical symptoms of cardiac ischemia with myocardial necrosis). We use microrray to identify changes in pathways following MI.This study examines mRNA expression levels in human whole blood at 7 and 30 days post ACS. Patients with MI are compared to those with UA (not healthy controls), thus focusing on differences in mRNA expression due to the acute clinical events rather than underlying atherosclerosis and its treatment. We recruited 26 patients presenting with acute coronary syndromes (ACS); 8 with unstable angina (UA) and 18 with MI. Supplementary files: The files contain the combined values (for each group) of the single patients' expression levels, the fold changes and the significance levels associated. Gene expression levels were estimated using probabilistic models implemented in puma (Propagating Uncertainty in Microarray Analysis, bioconductor.org), which provide estimates for the variance and credibility interval for probe level errors of each transcript. FCs were calculated after combining gene expression values within groups using Bayesian hierarchical model, incorporating probe level errors into the variance estimate. Significance levels for differentially expressed genes were detected by calculating the probability of positive log ratio (PPLR). The higher is the probability the more confident is the estimate of that positive FC, conversely the lower is the probability the more confident is the estimate of that FC to be negative. This model was implemented in the pumaComb and pumaDE modules within puma. file1 = mRNA_MI_combday30_exprs file2 = mRNA_MI_combDay7_exprs
2011-05-06 | E-GEOD-29111 | biostudies-arrayexpress
Project description:We aim to determine blood transcriptome-based molecular signature of acute coronary syndrome (ACS), and to identify novel serum biomarkers for early stage ST-segment-elevation myocardial infarction (STEMI) We obtained peripheral blood from the patients with ACS who visited emergency department within 4 hours after the onset of chest pain: ST-elevation myocardial infarction (STEMI, n=7), Non-ST-elevation MI (NSTEMI, n=10) and unstable angina (UA, n=9), and normal control (n=7)
2015-05-23 | E-GEOD-60993 | biostudies-arrayexpress
Project description:Sexual dimorphisms are well recognized in various cardiac diseases, including myocardial infarction (MI). MI develops later in women, but once established, it contributes more persistent symptoms and higher mortality than in men. Similar observations have been reported in murine model of MI. Although mRNA-level sexual dimorphism of MI have been reported, whether miRNA transcriptome also confers such dimorphism remains unknown. Comprehensive understanding of the mRNA- and miRNA-level genetic programs underlying the heart sexual dimorphisms will expectedly improve clinical outcome by facilitating the development of gender specific treatment strategies. Here, by conducting miRNA microarray analysis of murine MI model samples, we set out to characterize the heart sexual dimorphisms at the level of miRNA transcriptome The left anterior descending (LAD) coronary artery of mice aged 10 weeks was surgically ligated to create extensive MI. The ventricular septum of the areas at risk of ischemia was sampled on post-operative day 28. Total RNA was extracted using Sepasol solution (Sepasol-RNA I super G, nakalai tesque, Japan), and microarray analysis was performed using Affymetrix GeneChip® miRNA 3.0 Arrays
2016-01-07 | E-GEOD-76592 | biostudies-arrayexpress
Project description:Acute coronary syndrome (ACS) is presented as a group of symptoms resulting from acute ischemia of the myocardium due to rupture of a coronary arterial plaque. It comprises different classes; unstable angina, STEMI and NSTEMI. The current cornerstones of ACS diagnosis are ECG, CK-MB and cardiac troponins however there are several limitations leading to evading early diagnosis and poor prognosis. This highlights the need for more sensitive and specific biomarkers for a better outcome. In this study,an initial screening set is RNA sequenced for retrieval of differentially expressed genes and miRNAs. Then, a microRNA-long non-coding RNA multi biomarker panel is retrieved via in silico data analysis related to PINK1/Parkin-induced mitophagy. This is followed by clinical validation of their expression in serum of ACS patients in comparison to non-cardiac chest pain patients and healthy volunteers via qRT-PCR.
2023-01-01 | GSE202937 | GEO
Project description:We established a rat model of myocardial Infarction by performing a surgical operation of left anterior descending coronary artery occlusion under sterie conditions. Wistar rats were previously randomly divided into 4 groups: control, ischemia, ischemia-propranolol, and non-ischemia-propranolol. Our data suggested that propranolol could reverse many microRNAs with too high or too low expression in the ischemia group versus control group. Wistar rats were initially anesthetized with pentobarbital (40 mg/kg, i.v.), which were previously randomly divided into 4 groups: control, ischemia (MI), ischemia-propranolol (MI-PRO), and non-ischemia-propranolol (NMI-PRO). The rat model of MI was established by performing a surgical operation of left anterior descending coronary artery occlusion under sterie conditions. Successful occlusion was confirmed by an increase in the amplitude of R wave of lead I during the first few seconds of each occlusion and elevation of S-T segment of lead II, and a 20-30% decline in the arterial blood pressure compared to the pre-ischemic values mesured by a previously installed ECG recorder (BL 420, ChengDu TME Technology Co, Ltd, ChengDu, China). Propranolol was administrated 2 months before the experiment with daily oral doses of 50 mg/kg. Hearts were quickly isolated after the rats were sacrificed and the ischemic zone of the left ventricle was prepared for the miRNA microarray experiment. Control and NMI-PRO animals underwent open chest procedures without coronary artery occlusion.
2010-06-19 | E-GEOD-18129 | biostudies-arrayexpress
Project description:Background–Acute coronary syndrome (ACS) is sometimes accompanied by accelerated coagulability, lipid metabolism, and inflammatory responses, which are not attributable to the cardiac events alone. We hypothesized that the liver plays a pivotal role in the pathophysiology of ACS. We simultaneously analyzed the gene expression profiles of the liver and heart during acute myocardial ischemia in mice. Methods and Results–Mice were divided into three treatment groups: sham-operation, ischemia-reperfusion (I/R), and myocardial infarction. Mice with liver I/R were included as additional controls. Marked changes in hepatic gene expression were observed after 24 hours, despite the lack of histological changes in the liver. Genes related to tissue remodeling, adhesion molecules, and morphogenesis were significantly upregulated in the livers of mice with myocardial I/R or infarction, but not in those with liver I/R. Myocardial ischemia, but not changes in the hemodynamic state, was postulated to significantly alter hepatic gene expression. Moreover, detailed analysis of the signaling pathway suggested the presence of humoral factors that intervened between the heart and liver. To address these points, we utilized isolated primary hepatocytes and showed that osteopontin released from the heart actually altered the signaling pathways of primary hepatocytes to those observed in the livers of mice under myocardial ischemia. Moreover, osteopontin stimulated primary hepatocytes to secrete vascular endothelial growth factor-A, which is important for tissue remodeling. Conclusions– Hepatic gene expression is potentially regulated by cardiac humoral factors under myocardial ischemia. These results provide new insights into the pathophysiology of ACS.
2009-11-12 | GSE14843 | GEO
Project description:We have employed whole genome microarray expression profiling as a discovery platform to identify genes involved in plaque rupture. Human coronary artery endothelial cells (ECs) were stimulated in vitro for 12 hours with plasma obtained from the coronary sinus (CS) and the aorta (Ao) of patients with ACS (n=8), or patients with stable angina (SA, n=4). For each patient, gene expression profile was evaluated by microarray technology in ECs exposed to plasma obtained from CS and compared to that of ECs exposed to plasma sampled from Ao. In patient with ACS we found 684 genes up-regulated and 283 down-regulated was observed as compared to patients with SA. Functional and network analyses of statistically significant gene showed that the up regulated genes were associated to pathways IL17 Signaling. To validate the microarray data the RNAs were used for Real Time PCR experiment. Human coronary artery endothelial cells (ECs) were stimulated in vitro for 12 hours with plasma obtained from the coronary sinus (CS) and the aorta (Ao) of patients with ACS (n=8), or patients with stable angina (SA, n=4). For each patient, gene expression profile was evaluated by microarray technology in ECs exposed to plasma obtained from CS and compared to that of ECs exposed to plasma sampled from Ao.
2014-02-14 | E-GEOD-54977 | biostudies-arrayexpress
Project description:Heart failure (HF) is the most common cause of morbidity and mortality in the developed countries, especially considering the present demographic tendencies in those populations. We identified biologically relevant transcripts that are significantly altered in the early phase of myocardial infarction (MI) and are associated with the development of post-myocardial infarction HF. We collected peripheral blood samples from patients (n=111) with ST-segment elevation myocardial infarction (STEMI) at four time points (admission, discharge, 1 month after MI, and 6 months after MI). Control group comprised patients (n=46) with a stable coronary artery disease and without a history of myocardial infarction. Affymetrix HuGene 1.0 ST arrays were used to analyze mRNA levels in periperal blood mononuclear cells (PBMCs) isolated from the study and control groups. Samples from the first three time points were compared with the samples from the same patients collected 6 months after MI (stable phase) and with the control group. Additionaly, based on plasma NT-proBNP level and left ventricular ejection fraction parameters the STEMI patients were divided into HF and non-HF groups.We attempted to identify transcripts whose differential expression on the 1st day of myocardial infarction predicted which patients would develop symptoms of HF during the 6 months of follow-up. For this purpose, we compared the microarray results for samples collected on admission for the HF group versus the non-HF group.
2015-05-21 | E-GEOD-59867 | biostudies-arrayexpress
Project description:We aim to determine blood transcriptome-based molecular signature of acute coronary syndrome (ACS), and to identify novel serum biomarkers for early stage ST-segment-elevation myocardial infarction (STEMI) We obtained peripheral blood from the patients with ACS who visited emergency department within 4 hours after the onset of chest pain: a set of blood samples of patients with STEMI (n=7) before and 7 days after the primary percutaneous coronary intervention (n=7) and normal control (n=10)
2015-05-23 | E-GEOD-61144 | biostudies-arrayexpress
Project description:Myocardial infarction (MI) is the leading cause for hear failure (HF). Following MI, the non-infarcted region of left ventricle (LV) is critical for maintaining heart function, and disruption of the LV contributes greatly to post-MI HF. Transcriptomic profiling by high-throughput sequencing was performed in a chronic HF pig model, to explore the molecular changes in the post-MI LV related to cardiovascular deterioration. Samples were taken from heart tissue of MI-induced pigs and from control pigs not subjected to MI. Regions of the heart where samples were taken included the site of ischemia (LV ischemia), area bordering ischemia (LV border), area remote to ischemia (LV remote) and the right ventricle (RV).
2021-10-04 | E-MTAB-8856 | biostudies-arrayexpress