Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA371776 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5237680_1.fastq.gz | Fastqsanger.gz | |||
| SRR5237680_2.fastq.gz | Fastqsanger.gz | |||
| SRR5237681_1.fastq.gz | Fastqsanger.gz | |||
| SRR5237681_2.fastq.gz | Fastqsanger.gz | |||
| SRR5237682_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 24 |
Similar Datasets
Project description:Many different subsets of smooth muscle cells (SMC) are present in advanced atherosclerotic plaque. We used single cell sequencing to interrogate the impact of MCP1 made by Lgals+ smooth muscle cells on smooth muscle and immune cell subsets in advanced atherosclerotic plaque
2022-07-30 | GSE204994 | GEO
Project description:In response to various stimuli, vascular smooth muscle cells (SMCs) can de-differentiate, proliferate and migrate in a process known as phenotypic modulation. However, the phenotype of modulated SMCs in vivo during atherosclerosis and the influence of this process on coronary artery disease (CAD) risk have not been clearly established. Using single cell RNA sequencing, we comprehensively characterized the transcriptomic phenotype of modulated SMCs in vivo in atherosclerotic lesions of both mouse and human. We performed CITE-seq in mouse atherosclerotic lesions using antibodies directed against several macrophage surface markers. In the mice, we also performed SMC-specific knockout of TCF21, a causal CAD gene, to determine the effect of this gene on SMC phenotypic modulation. Finally, we performed ChIP-seq for the transcription factor TCF21 in a pooled DNA sample comprised of 52 different human coronary artery smooth muscle cell (HCASMC) lines to determine TCF21 target genes.
2019-07-29 | GSE131778 | GEO
Project description:In response to various stimuli, vascular smooth muscle cells (SMCs) can de-differentiate, proliferate and migrate in a process known as phenotypic modulation. However, the phenotype of modulated SMCs in vivo during atherosclerosis and the influence of this process on coronary artery disease (CAD) risk have not been clearly established. Using single cell RNA sequencing, we comprehensively characterized the transcriptomic phenotype of modulated SMCs in vivo in atherosclerotic lesions of both mouse and human. We performed CITE-seq in mouse atherosclerotic lesions using antibodies directed against several macrophage surface markers. In the mice, we also performed SMC-specific knockout of TCF21, a causal CAD gene, to determine the effect of this gene on SMC phenotypic modulation. Finally, we performed ChIP-seq for the transcription factor TCF21 in a pooled DNA sample comprised of 52 different human coronary artery smooth muscle cell (HCASMC) lines to determine TCF21 target genes.
2019-07-29 | GSE131776 | GEO
Project description:In response to various stimuli, vascular smooth muscle cells (SMCs) can de-differentiate, proliferate and migrate in a process known as phenotypic modulation. However, the phenotype of modulated SMCs in vivo during atherosclerosis and the influence of this process on coronary artery disease (CAD) risk have not been clearly established. Using single cell RNA sequencing, we comprehensively characterized the transcriptomic phenotype of modulated SMCs in vivo in atherosclerotic lesions of both mouse and human. We performed CITE-seq in mouse atherosclerotic lesions using antibodies directed against several macrophage surface markers. In the mice, we also performed SMC-specific knockout of TCF21, a causal CAD gene, to determine the effect of this gene on SMC phenotypic modulation. Finally, we performed ChIP-seq for the transcription factor TCF21 in a pooled DNA sample comprised of 52 different human coronary artery smooth muscle cell (HCASMC) lines to determine TCF21 target genes.
2019-07-29 | GSE131779 | GEO
Project description:In response to various stimuli, vascular smooth muscle cells (SMCs) can de-differentiate, proliferate and migrate in a process known as phenotypic modulation. However, the phenotype of modulated SMCs in vivo during atherosclerosis and the influence of this process on coronary artery disease (CAD) risk have not been clearly established. Using single cell RNA sequencing, we comprehensively characterized the transcriptomic phenotype of modulated SMCs in vivo in atherosclerotic lesions of both mouse and human. We performed CITE-seq in mouse atherosclerotic lesions using antibodies directed against several macrophage surface markers. In the mice, we also performed SMC-specific knockout of TCF21, a causal CAD gene, to determine the effect of this gene on SMC phenotypic modulation. Finally, we performed ChIP-seq for the transcription factor TCF21 in a pooled DNA sample comprised of 52 different human coronary artery smooth muscle cell (HCASMC) lines to determine TCF21 target genes.
2019-07-29 | GSE131777 | GEO
Project description:Atherosclerotic plaque rupture with subsequent embolic events is a major cause of sudden death from myocardial infarction or stroke. Although smooth muscle cells (SMC) produce and respond to collagens in vitro, there is no direct evidence in vivo that SMC are a critical source of collagens impacting lesion development or fibrous cap formation. We sought to determine how conditional SMC specific knockout of collagen type XV (COL15A1) in SMC lineage tracing mice effects advanced lesion formation. COL15A1 was chosen because: 1) we previously identified a Col15a1 sequence variant associated with age related atherosclerosis; 2) COL15A1 is a matrix organizer that enhances tissue structural integrity; and 3) siRNA mediated Col15a1 knockdown increased migration and decreased proliferation of SMC in vitro. We hypothesized that SMC derived COL15A1 is critical in advanced lesion pathogenesis and fibrous cap formation. Surprisingly, we demonstrate that SMC specific Col15a1 knockout mice fed a Western diet for 18 weeks failed to form advanced lesions. SMC Col15a1 knockout lesions have a drastic reduction in overall lesion size, cell accumulation, and the absence of a SMC and ECM- rich lesion or fibrous cap. In vivo RNA-seq analysis on lesions +/- SMC Col15a1 knockout suggests the mechanism for these effects is complex and associated with reductions in multiple pro-atherogenic inflammatory pathways in multiple cell types involved in lesion development. These results thus provide the first direct evidence that a SMC derived collagen is critical during lesion pathogenesis. Additionally, we conclude that SMC Col15a1 knockout unexpectedly inhibited rather than exacerbated lesion pathogenesis.
2017-09-08 | GSE94661 | GEO
Project description:Cardiovascular disease is the leading cause of death in developed countries and there is compelling evidence that the majority of these fatalities are secondary to rupture of unstable atherosclerotic plaques. However, the mechanisms that control plaque stability are poorly understood, although it is widely believed that plaques having a decreased ratio of cells positive for smooth muscle cell (SMC) markers such as ACTA2 relative to macrophage markers are more likely to rupture. Herein we employMyh11-CreERT2 ROSA floxed STOP eYFP Apoe-/- mice to trace SMC lineage and show that traditional methods for detecting SMCs based on immunostaining for SMC markers like ACTA2 are unable to detect 82% of SMC-derived cells within advanced atherosclerotic lesions. Moreover, we show that these SMC-derived cells within advanced lesions exhibit multiple phenotypes including activation of multiple markers of macrophages, mesenchymal stem cells (MSC), and myofibroblasts (MF). Importantly, we show that SMC-derived macrophage like cells are phagocytic based on electron microscope YFP immunolabeling. In addition, results of single cell epigenetic assays developed in our lab shows that nearly 20% of macrophage-like cells within human lesions are of SMC not myeloid origin. These phenotypic transitions appear to be critical in lesion pathogenesis, in that we show that SMC-specific conditional knockout (KO) of the pluripotency factor, Krüppel-like factor 4 (KLF4), resulted in marked reductions in lesion size, increases in multiple indices of plaque stability, and reduced numbers of SMC-derived MSC- and macrophage-like cells. Finally, we show that cholesterol loading of cultured SMC is associated with activation of multiple markers of macrophages and MSC, secretion of pro-inflammatory cytokines, and increased phagocytosis, all of which are Klf4 dependent. Taken together, results indicate that the contribution of SMCs within atherosclerotic plaques has been greatly underestimated, and that loss of Klf4 within SMC result in major changes in SMC phenotype and function that play a major role in lesion pathogenesis. Examination of KLF4 transcription factor in an atherosclerosis setting
2015-04-24 | E-GEOD-65812 | biostudies-arrayexpress
Project description:Expression levels of the RNA-binding protein Quaking (QKI) are low in monocytes of early, human atherosclerotic lesions, but abundant in macrophages of advanced plaques. Specific depletion of QKI protein impaired monocyte adhesion, migration, differentiation into macrophages, and foam cell formation in vitro and in vivo. RNA-seq and microarray analysis of human monocyte and macrophage transcriptomes, including those of a unique QKI haploinsufficient patient, revealed striking changes in QKI-dependent mRNA levels and splicing of RNA transcripts. RNA-seq analysis of primary monocytes and macrophages from a QKI haploinsufficient patient and their (control) sibling.
2016-01-04 | E-GEOD-74978 | 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. Laser captured smooth muscle cells and macrophages from carotid plaque sections (n=3) profiled in the Merck/Agilent 44k v1.1. The reference sample was a pool RNA from whole sections.
2011-09-30 | E-GEOD-23303 | biostudies-arrayexpress
Project description:IL-1 plays an important role in atherosclerosis, and alters expression of a number of genes involved in atherosclerotic plaque development and progression. Smooth muscle cells play important roles in atherosclerotic plaque formation and stability, so this study was undertaken to determine the global effects of IL-1b on gene expression in smooth muscle cells in vitro. Cultured rat aortic smooth muscle cells were treated with IL-1b (2.5 ng/mL) or vehicle (0.1% BSA) for 24 hours prior to harvest.
2012-12-31 | E-GEOD-21403 | biostudies-arrayexpress