Differential gene expression along with progression of diet-induced atherosclerotic plaque using Microarray
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE55796 | GEO | 2014/03/12
SECONDARY ACCESSION(S): PRJNA241033
REPOSITORIES: GEO
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Project description:To understand the changes in microRNA expression regulating specific genes 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.
2016-11-16 | GSE89858 | GEO
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
2014-03-12 | E-GEOD-55796 | biostudies-arrayexpress
Project description:Atherosclerosis is modulated by immune cells. Understanding the diversity and heterogeneity in the aorta in steady state, as well as during different stages of disease will help to determine mechanisms promoting disease progression. To characterize the immune cells, we performed single cell RNA sequencing of aortic CD45+ leukocytes from C57BL/6 (WT) on chow diet and early disease Ldlr-/- mice fed high fat diet (HFD) for 21-days. The single cell RNA-seq analyses revealed the heterogeneity of aortic macrophages in steady state and early atherosclerotic disease.
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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.
2023-05-10 | PXD030857 | Pride
Project description:This SuperSeries is composed of the following subset Series: GSE23303: Gene expression profiling of human atherosclerotic plaque: Laser capture microscopy of smooth muscle cells and macrophages GSE23304: Gene expression profiling of human atherosclerotic plaque: 101 peripheral plaques GSE24495: Gene expression profiling of human atherosclerotic plaque: Carotid plaque GSE24702: Gene expression profiling of human atherosclerotic plaque: 290 peripheral plaques Refer to individual Series
2011-09-30 | E-GEOD-23314 | biostudies-arrayexpress
Project description:Dysregulation of lipid metabolism is the pathological basis of the occurrence and development of atherosclerosis.The pig is an ideal animal to study human cardiovascular diseases. However, the specific changes of lipid metabolism in its atherosclerotic plaques, as well as the underlying mechanisms, remain to be elucidated. To investigate the alterations of lipid metabolism related pathways, especially ceramide synthesis related genes, in the abdominal aorta of atherosclerotic pigs induced by high-fat, high-cholesterol, and high-fructose (HFCF) diet, we performed RNA-Seq on abdominal aorta tissue from Wuzhishan pigs fed either normal chow diet or HFCF diet for six months.
2024-01-31 | GSE245530 | GEO
Project description:Aberrantly expressed miRNAs contribute to developmental abnormalities and diseases such as cancer, diabetes, and cardiovascular disorders, by hybridizing to specific mRNA targets and repressing their translation into proteins. Although miRNA expression signature is characterized in the process of neointimal thickening during proliferative vascular diseases such as atherosclerosis, so far global miRNA expression profiling in the different stages of atherosclerosis is completely unknown. We explored stage-specific microRNA signatures in the progress of atherosclerosis in hyperlipidemia mouse model, which may help to identify the critical miRNAs contributing atherosclerotic development and stabilization. Female apoe-/- mice (6-8 weeks, Jackson Laboratory) were fed a high fat diet (HFD, 21% crude fat, 0.15% cholesterol and 19.5% casein, Altromin, Germany) for 3 or 10 months (N=3-4). Serial sections (20 µm thick) of aortic roots and carotid arteries from these mice were mounted on membrane mounted metal frame slides (MMI), deparaffinized under RNase-free conditions, and completely dried. Laser capture microdissection (LCM) was performed with a laser microdissection system (MMI cellcut plus, Molecular Machines and Industries, Switzerland) assembled onto an inverted microscope (Olympus IX71). Plaque tissue or morphologically normal vessel wall of at least 40 sections per mouse were collected. RNA was isolated using RecoverAll total nucleic acid isolation kit (Applied Biosystems) according to the manufacturer’s instructions.
2013-03-27 | E-GEOD-34647 | biostudies-arrayexpress
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)
2011-09-30 | E-GEOD-24495 | 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
2009-01-16 | GSE11138 | GEO
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.
2011-10-01 | GSE24495 | GEO