Differential microRNA expression along with progression of diet-induced atherosclerotic plaque using Microarray
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE89858 | GEO | 2016/11/16
SECONDARY ACCESSION(S): PRJNA354259
REPOSITORIES: GEO
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Project description:To understand the changes in gene expression at different stages of diet-induced atherosclerotic development, double knock out Apobtm2Sgy/Ldltm1Her mice were fed with either high-fat or normal chow diet. The microarray was performed using total RNA extracted from ascending aorta of the animals. Double knockout mice fed with rich cholesterol diet and a normal diet were sacrificed after 0, 4, 8, 14 and 20 weeks and RNA was extracted for Microarray analysis
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Project description:In order to identify potential new biomarkers of atherosclerotic plaque composition we performed a large scale analysis of gene expression patterns in human atherosclerotic lesions. Whole genome expression analysis of 101 peripheral plaques identified a robust gene signature (1514 genes) dominated by inflammatory processes, and cholesterol metabolism and storage genes. Specific pathways enriched in this signature included activation of the Toll-like receptor signaling pathway, T-cell activation, cholesterol efflux, oxidative stress response, inflammatory cytokine production, vasoconstriction and lysosomal activity. Analysis of gene expression in plaque micro-dissected material revealed that the signature is strongly up-regulated in macrophage-rich regions and down-regulated in regions with high smooth muscle cell content. A smaller qPCR biomarker panel and inflammatory composite score (ICS) were developed to facilitate clinical translation of discoveries from gene expression profiling. We found that ICS correlates with histological features related to plaque vulnerability. In addition, ICS is able to separate groups of plaques obtained from symptomatic and asymptomatic patients undergoing carotid endarerectomy. In summary, we identified a robust mRNA biomarker panel associated with histo-pathological as well as clinical hallmarks of vulnerable atherosclerotic plaque. This panel may be used as a diagnostic and prognostic tool in clinical setting to evaluate novel anti-atherosclerotic therapies. 6 human carotid plaques were sectioned in 1 mm thick slices. Alternative slices were used for gene expression profiling in Affymetrix/Merck custom 1.0 arrays (GPL10687), or for immunohistochemistry studies (CD68, Actin)
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2013-03-27 | E-GEOD-34647 | biostudies-arrayexpress
Project description:We used microarray analyses in human atherosclerotic plaque to identify network imply in the maintenance and progression of the pathology. To obtain a wide dynamic range we used the scanning method proposed by Skibbe et al. (Bioinformatics. 2006;22(15):1863-1870) performing three subsequent scansions for the same slide. We performed before low than medium and high PMT and laser intensity scansions to permit to detect differences in expression of high expressed genes from the first scansion and from low expressed genes from the last scansion. Data were total and lowess normalized, filtered and used to detect differentially expressed genes separately (low, medium and high). Differentially expressed genes were than integrated. Our data enhance the importance of both the inflammatory stress responses, controlled by central node STAT1 (inducing also the over-expression of the heat shock proteins HSP47 and HO-1), and caveolae system related to steroid hormone receptors. Since atherosclerosis affects aorta, coronary, carotid, and iliac arteries most frequently than any other body vessel there may be common molecular pathways involved in sustenance of this process. We integrated our DNA microarrays data with plaque carotid gene expression (Array Express databases E-MEXP-268) by meta-analysis method. We identified a series of common potential human atherogenic genes and were able to integrate them in functional networks involved in atherosclerosis. Activation of the JAK/STAT pathway was confirmed by the up-regulation of IL-6, STAT1, ISGF3G and IL10RA genes in coronary and carotid plaques. These results and constructed functional network could be related to a central role for STAT protein and caveolae system to regulate the hypertension state. Keywords: disease state analysis, Plaque atherosclerotic, LAD coronary
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Project description:In order to identify potential new biomarkers of atherosclerotic plaque composition we performed a large scale analysis of gene expression patterns in human atherosclerotic lesions. Whole genome expression analysis of 101 peripheral plaques identified a robust gene signature (1514 genes) dominated by inflammatory processes, and cholesterol metabolism and storage genes. Specific pathways enriched in this signature included activation of the Toll-like receptor signaling pathway, T-cell activation, cholesterol efflux, oxidative stress response, inflammatory cytokine production, vasoconstriction and lysosomal activity. Analysis of gene expression in plaque micro-dissected material revealed that the signature is strongly up-regulated in macrophage-rich regions and down-regulated in regions with high smooth muscle cell content. A smaller qPCR biomarker panel and inflammatory composite score (ICS) were developed to facilitate clinical translation of discoveries from gene expression profiling. We found that ICS correlates with histological features related to plaque vulnerability. In addition, ICS is able to separate groups of plaques obtained from symptomatic and asymptomatic patients undergoing carotid endarerectomy. In summary, we identified a robust mRNA biomarker panel associated with histo-pathological as well as clinical hallmarks of vulnerable atherosclerotic plaque. This panel may be used as a diagnostic and prognostic tool in clinical setting to evaluate novel anti-atherosclerotic therapies.
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