Expression data from normal human and unstable angina patient.
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Xiaojuan Ma
PROVIDER: E-GEOD-34781 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:20 patients with unstable angina were divided into patient group by using coronary angiography. The sex- and age-matched healthy individuals were enrolled as control group. Venous bloods were collected for extracting RNA.
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Project description:This study describes a circulating miRNA signature of unstable angina (UA), which may be used as a novel biomarker for unstable coronary artery disease (CAD). The Taqman low-density miRNA array were used to identify distinct miRNA expression profiles in the plasma of patients with typical UA and angiographically documented CAD (UA group, n = 13) compared to individuals with non-cardiac chest pain (control group, n = 13).
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Project description:This study describes a circulating miRNA signature of unstable angina (UA), which may be used as a novel biomarker for unstable coronary artery disease (CAD). The Taqman low-density miRNA array were used to identify distinct miRNA expression profiles in the plasma of patients with typical UA and angiographically documented CAD (UA group, n = 13) compared to individuals with non-cardiac chest pain (control group, n = 13). EDTA-plasma samples were obtained before the cardiac catheterization procedure.The study included 2 groups that were classified according to angiographic evidence and clinical evaluation of chest pain. Patients with chest pain or discomfort but with angiographic exclusion of coronary atherosclerosis were enrolled in the control group (n = 13). Chest discomfort referred to the following complaints: chest pain, pressure, tightness, or heaviness; pain that radiated to the neck, jaw, shoulders, back, or one or both arms; and persistent shortness of breath. Patients with typical unstable angina (UA) and angiographically documented CAD were enrolled in the UA group (n = 13).
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Project description:We profiled miRNA expression in the plasma from healthy subjects and patients with unstable angina pectoris to obtain differentially expressed plasma miRNAs. We randomly selected 25 samples from each group and combined into a sample pool. In this way we obtained 7 and 6 sample pools in control group and case group, respectively. miRNA levels in the plasma were detected with miRCURY LNATM microRNA Array, 6th gen -hsa, mmu & rno.
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Project description:Expression data from normal human and unstable angina patient.
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Project description:Transcriptional profiling of stable and unstable atherosclerotic plaque segments from human carotid endatrerectomies Objective Comparison of gene expression in stable versus unstable atherosclerotic plaque may be confounded by interpatient variability. The aim of this study was to identify differences in gene expression between stable and unstable segments of plaque obtained from the same patient. Human carotid endarterectomy specimens were segmented and macroscopically classified using a morphological classification system. Two analytical methods, an intraplaque and an interplaque analysis, revealed 170 and 1916 differentially expressed genes, respectively using Affymetrix gene chip analysis. A total of 115 genes were identified from both analyses. The differential expression of 27 genes was also confirmed using quantitative-polymerase chain reaction on a larger panel of samples. Eighteen of these genes have not been associated previously with plaque instability, including the metalloproteinase, ADAMDEC1 (37-fold), retinoic acid receptor responder-1 (5-fold), and cysteine protease legumain (3-fold). Matrix metalloproteinase-9 (MMP-9), cathepsin B, and a novel gene, legumain, a potential activator of MMPs and cathepsins, were also confirmed at the protein level. The differential expression of 18 genes not previously associated with plaque rupture has been confirmed in stable and unstable regions of the same atherosclerotic plaque. These genes may represent novel targets for the treatment of unstable plaque or useful diagnostic markers of plaque instability. Differential gene expression in stable and unstable plaque was assessed by whole transcriptome analysis. Intraplaque analysis by QT-PCR confirmed the differential expression of 18 genes not associated previously with plaque rupture. These genes may represent novel targets for the treatment of unstable plaque or useful diagnostic markers of plaque instability
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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.
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Project description:The rupture of unstable atherosclerotic plaques, leading to debilitating or fatal thrombotic events, is a major health burden worldwide. Limited understanding as to the molecular drivers of plaque instability and rupture hinders efforts in diagnosis and treatment prior to thrombotic events. Utilising an advanced pre-clinical mouse model (Tandem stenosis (TS) model), which presents human-like unstable atherosclerotic disease, we apply high-end omic methods to characterize the molecular signatures associated with plaque instability in atherosclerotic arteries. Through quantitative proteomic profiling, we depict unique proteome signatures of unstable plaques compared to stable plaques and healthy arteries. Coupled with single-cell RNA-sequencing of leukocytes, we describe the heterodimer complex S100a8/S100a9 as unique to unstable plaque, with neutrophils implicated as the transcriptional drivers of S100a8/a9 expression. We confirm S100a9 expression in human carotid atherosclerotic plaques and we further utilise the TS pre-clinical model to pharmacologically inhibit S100a8/S100a9, resulting in plaque stabilisation. Thus, we establish the TS model as a sophisticated translational tool for the profiling of unstable atherosclerotic plaques and demonstrate that unstable and stable atherosclerosis are highly different disease entities.
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Project description:Four male patients were enrolled for this study in collaboration with the Cardiology Unit of Policlinico Tor Vergata-Fondazione PTV (Rome). We have performed RNA-Sequencing using NextSeq 500 ILLUMINA platform on PBMCs of patients with clinically proven healthy coronary arteries (CTR) and patients with chronic coronary artery disease (CAD) confirmed by coronary angiography. RNA sequencing results showed differentially Altenative Splicing (AS) events and filtering for a statistically significant Splicing-Index Fold-Change≥ ±1.5 (p≤0.05) we observed 113 differentially regulated AS events (24 up and 89 down-regulated) from 86 genes. We validated AS results using Real-time PCR method and then we extended the expression analysis to a large case study including 24 CTR subjects, 72 CAD patients and 32 patients with unstable coronary artery disease, arrived at the attention of the clinicians during a myocardial infarction event (AMI group).
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