Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA156367 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:MiRNA expression profile in murine early atherosclerotic plaque compared with un-diseased arterial tissue
| PRJNA156369 | ENA
Project description:MiRNA expression profile in murine advanced atherosclerotic plaque compared with early atherosclerotic plaque
| PRJNA156365 | ENA
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:The accumulation of lipid-laden macrophages (foam cells) in the arterial wall is a crucial early step in atherosclerotic plaque development. Modified low-density lipoprotein (LDL) is the primary cholesterol source for foam cells, taken up in an unregulated manner through scavenger receptors. This type of cells exhibit reduced migratory capacity while producing elevated levels of pro-inflammatory cytokines, thereby promoting inflammation and plaque progression. Still our understanding of the transcriptomic changes during macrophage-to-foam cell conversion remains limited. In this experiment, we aimed to identify genes responsible for the accumulation of cholesterol in human monocyte-derived macrophages exposed to modified and native LDL. The monocyte samples collected from healthy individuals were purified and exposed to modified and native LDLs obtained from plasm of atherosclerotic patients. RNA extracted after 24h of incubation was sequenced with polyA selection. The resulting data was normalised with limma and undergone DEG analysis followed by upstream analysis workflow with TRANSPATH and TRANSFAC databases to discover master regulator molecules.
2023-08-14 | E-MTAB-13261 | biostudies-arrayexpress
Project description:Despite unprecedented advances in the treatment of atherosclerotic cardiovascular diseases (CVD), it remains the leading cause of death in patients with diabetes worldwide. Lipid-laden atherosclerotic plaque development within the arterial vessel wall is initiated with endothelial cell activation, monocyte adhesion and foam cell formation. Although the current focus has been on mitigation of risk factors, the disease continues to progress, and thus newer approaches and druggable targets need to be identified that can directly inhibit the underlying pathobiology of atherosclerosis. We utilised a single cell RNA sequencing (scRNA-seq) approach to distinguish the proatherogenic transcriptional profile of aortic cells in diabetes.
2024-09-09 | GSE211216 | GEO
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: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:Background Rupture or erosion of advanced atherosclerotic lesions with a resultant myocardial infarction or stroke are the leading worldwide cause of death. However, we have a very limited understanding of the identity, origin, and function of many cells that make up late stage atherosclerotic lesions, as well as the mechanisms by which they control plaque stability. Methods and Results Using RNAseq and ChIPseq of advanced atherosclerotic lesions from mice, we provide evidence SMC-specific Klf4- versus Oct4-knockout ApoE-/- mice showed virtually opposite genomic signatures and putative SMC Klf4 or Oct4 target genes play an important role regulating SMC phenotypic changes. Further, we conducted a comprehensive single-cell RNA-seq of advanced human carotid endarterectomy samples and compared these with scRNAseq from murine micro-dissected advanced atherosclerotic lesions with SMC and endothelial lineage tracing to survey all plaque cell types and rigorously determine their origin. This analysis revealed remarkable similarity of transcriptomic clusters between mouse and human lesions and extensive plasticity of SMC- and EC-derived lesion cells. The latter included 7 distinct clusters of SMC- and EC-derived cells, most negative for traditional markers. In particular, SMC contributed to a Myh11-, Lgals3+ population with a chondrocyte-like gene signature that was markedly reduced with SMC-specific conditional knockout of Klf4. To study these cells and the mechanisms of their transition, we developed an innovative dual lineage tracing mouse that can uniquely label and genetically target Myh11+ SMC that subsequently activate Lgals3. We observed that SMC that activate Lgals3 comprise up to 2/3 of all SMC in advanced plaques. However, initial activation of Lgals3 in these cells does not represent conversion to a terminally differentiated state, but rather represents transition of these cells to a unique stem cell marker gene+, ECM-remodeling, “pioneer” cell phenotype that are the first to invest within lesions and subsequently give rise to at least 3 other SMC phenotypes within advanced lesions including Klf4-dependent osteogenic phenotypes likely to contribute to plaque calcification and plaque destabilization. Conclusions Taken together, these results provide evidence that SMC-derived cells within advanced mouse and human atherosclerotic lesions exhibit far greater phenotypic plasticity than generally believed, with Klf4 regulating transition to multiple phenotypes including Lgals3+ osteogenic cells likely to be detrimental for late stage atherosclerosis plaque pathogenesis.
2020-07-23 | GSE150644 | GEO
Project description:miRNA expression profiling for human normal arterial intimae and advanced atherosclerotic plaques
| PRJNA941796 | ENA
Project description:The rupture of unstable atherosclerotic plaques, leading to debilitating or fatal thrombotic events, are a major health concern worldwide. Limited understanding as to the molecular drivers of plaque destabilisation and rupture hinders efforts in diagnosis and treatment prior to thrombotic events. Using an advanced pre-clinical model (tandem stenosis), we characterise the molecular signatures associated with plaque instability in atherosclerotic vessels.
2023-07-24 | PXD018224 | Pride