Profiles of microRNA expression of atherosclerotic plaques
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: zhang qy
PROVIDER: E-MTAB-2460 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:The Total RNA from seven control pool and seven atherosclerotic plaque sample pools were labeled by Cy3/Cy5 respectively and analyzed on 22K human genome array chip V1.0.
2015-02-20 | E-MTAB-2458 | biostudies-arrayexpress
Project description:We compared gene expression profiles between asymptomatic and symptomatic atherosclerotic plaques from the same patient. This was accomplished by analyzing carotid plaques from four patients with bilateral high-grade carotid artery stenoses one being symptomatic (TIA or stroke) and the other asymptomatic.
2006-02-10 | E-MEXP-268 | biostudies-arrayexpress
Project description:A microarray analysis of advanced human atherosclerotic carotid artery plaques (equal or over 70% stenosis, NASCET criteria) from radiologically confirmed ipsilateral stroke patients (stroke-susceptible plaques, n=12) compared with carotid plaques collected from clinically asymptomatic patients with clear brain imaging (asymptomatic plaques, n=9) with equivalent conventional risk factors and severity of carotid stenosis.
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Project description:We quantified differential microRNA (miRNA) expression on human HDL before and after incubation with human coronary artery endothelial cells. These data were used to determine which miRNAs are altered on HDL (taken up or effluxed to) by human coronary artery endothelial cells. Each group had a n=4 and HDL-miRNA levels post incubations were compared to pre incubations with cells.
2014-02-27 | E-GEOD-53314 | biostudies-arrayexpress
Project description:Cardiovascular disease (CVD) is the leading cause of death, with atherosclerosis a major underlying cause. While often asymptomatic for decades, plaque destabilisation and rupture can arise suddenly and cause acute arterial occlusion or peripheral embolisation resulting in acute myocardial infarction, stroke and lower limb ischaemia. Hard plaques are typically considered as stable, and soft plaques as unstable. Extracellular matrix (ECM) remodelling can result in plaque destabilisation, but the mechanisms that drive the development of unstable lipid-rich plaques with a thin fibrous cap, versus stable fibrotic plaques with a thick cap, are not fully understood. We hypothesised that there would be significant differences in ECM composition between hard (stable) and soft (unstable and rupture-prone) plaques. We identified and quantified >46700 proteins, including 367 ECM proteins, with unprecedented coverage and high reproducibility. We identified 575 proteins with differential abundances between hard (stable) and soft (unstable) plaques. Proteins involved in inflammation and ECM remodeling, including multiple proteases were enriched, and ECM proteins decreased, in soft plaques. These data provide a unique insight into inflammatory mechanisms and ECM remodelling as an explanation for plaque destabilization. Furthermore they provide a first step towards identifying circulating biomarkers for individualised risk profiling of arteriosclerosis.
2024-01-15 | PXD039077 | Pride
Project description:Detection of the altered expression of inflammation associated genes in patients’ blood can provide information regarding the stage of atherosclerotic plaque without undergoing invasive procedures. In the current study, the expression levels of miRNAs within the early stage and advanced stage atherosclerotic plaques was compared with left internal mammary tissue. Each of these tissues was obtained from 8 patients (males-5, females-3), aged 55-80 years, undergoing coronary artery bypass grafting surgery. Total RNA was isolated using Qiagen miRNeasy Mini Kit. The RNAs from the similar tissue types of 4 patients were pooled together to make one sample for one batch to be sequenced. Similarly, the RNAs from the same tissue type of remaining 4 patients were pooled together to be used as second biological repeat for that tissue. Affymetrix GeneChip miRNA Array v. 4.0.platform was used to analyze miRNA expression.
2021-06-01 | E-MTAB-10051 | 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:Detection of the altered expression of inflammation associated genes in patients’ blood can provide information regarding the stage of atherosclerotic plaque without undergoing invasive procedures. In the current study, the expression levels of mRNAs within the early stage and advanced stage atherosclerotic plaques were compared with left internal mammary tissue. Each of these tissues was obtained from 8 patients (males-5, females-3), aged 55-80 years, undergoing coronary artery bypass grafting surgery. Total RNA was isolated using Qiagen miRNeasy Mini Kit. The RNAs from the similar tissue types of 4 patients were pooled together to make one sample for one batch to be sequenced. Similarly, the RNAs from the one tissue type of remaining 4 patients were pooled together to be used as second biological repeat for that tissue. Affymetrix GeneChip Human Transcriptome Array 2.0 platform was used to analyze the mRNA expression.
2021-06-01 | E-MTAB-10052 | biostudies-arrayexpress
Project description:Two different coronary artery samples with erosion plaques were selected from female heterozygous for the deletion BGN. Hybridization of target RNA-specific probes was used to visualize the spatial distribution of mutants. After determine the leison with clonality and non-clonal SMC proliferation, spatial transcriptomics was used to identify differentially expressed transcripts within clonal and non-clonal regions.
2023-12-04 | GSE243179 | GEO
Project description:BACKGROUND: Development of the neural tube is a highly orchestrated process relying on precise, spatio-temporal expression of numerous genes as well as hierarchies of signal transduction and gene regulatory networks. Disruption of expression of a number of genes participating in these networks is believed to underlie developmental anomalies such as neural tube defects (NTDs) resulting from anomalous neural tube morphogenesis. MicroRNAs (miRNAs), a large family of noncoding RNAs, have been shown to function as gene silencers, and thus, are key modulators of cell and tissue differentiation. To elucidate potential roles of miRNAs in murine neural tube development, miRNA gene expression profiling has been utilized in the current study, to garner novel and in-depth knowledge on the expression and regulation of genes encoding miRNAs as well as their potential target genes governing maturation of the mammalian neural tube. METHODS: With the aim of identifying differentially expressed miRNAs during mammalian neural tube ontogenesis, miRNA expression profiles from gestation day (GD) -8.5, -9.0 and -9.5 murine neural tube tissue were compared utilizing miRXplore™ microarrays from Miltenyi Biotech GmbH. Gene expression changes observed in microarray analysis were verified by TaqManTM quantitative Real-Time PCR. clValid R package and the UPGMA (hierarchical) clustering method were utilized for cluster analysis of the microarray data. Functional associations among selected miRNAs were examined exploiting Ingenuity Pathway Analysis. RESULTS: Expression of approximately 12% of the 609 murine miRNA genes examined was detected in murine neural tube tissues from GD -8.5, -9.0 and -9.5. Clustering analysis revealed several developmentally regulated clusters among these expressed genes. MicroRNA target analysis enabled identification of a panoply of protein-coding target genes of the differentially expressed miRNAs within such clusters. Interestingly, many of these target genes have been shown to be associated with vital cellular processes such as cell proliferation, cell adhesion, cell migration, differentiation, apoptosis and epithelial-mesenchymal transformation, all of which are essential for normal neural tube development. Utilization of Ingenuity Pathway Analysis (IPA; Ingenuity Systems) allowed identification of interactive biological networks connecting differentially expressed miRNAs and their target genes highlighting functional relationships. CONCLUSIONS: In the present study, a unique gene expression signature of a range of miRNAs in embryonic neural tube tissue was delineated. Analysis of miRNA target genes and gene interaction pathways emphasized that expression of numerous protein-encoding genes, indispensable for normal neural tube morphogenesis, may be regulated by specific miRNAs. Time-course experiment (Developmental Stages), ICR mice embryos on gestational days (GD) 8.5, 9.0 and 9.5. Biological replicates: For each day of gestation, 3 independent pools of 15 to 20 staged embryos were used to procure embryonic orofacial tissues for preparation of 3 distinct pools of RNA that were independently processed and applied to individual miRXplore™ microRNA Microarray chips (Miltenyi Biotec GmbH). Technology: 2-color spotted cDNA, Hy5 (experimental sample) vs. Hy3 (control - miRXplore Universal Reference).
2010-12-01 | E-GEOD-20879 | biostudies-arrayexpress