Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA156369 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:MiRNA expression profile in murine advanced atherosclerotic plaque compared with un-diseased arterial wall
| PRJNA156367 | ENA
Project description:MiRNA expression profile in murine advanced atherosclerotic plaque compared with early atherosclerotic plaque
| PRJNA156365 | ENA
Project description:MiRNA expression profile in murine un-diseased arterial tissue on 3 month high fat diet vs 10 month high fat diet
| PRJNA156191 | ENA
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:There is no effective pharmacotherapy to prevent the growth and rupture of abdominal aortic aneurysms (AAA), a leading cause of death. We developed a novel preclinical model showing that the interaction of bona fide risk factors (i.e., cigarette smoke (CS) and hypercholesterolemia) induced AAA formation, rupture, and death. Elastin fragmentation resulted from CS-induced exacerbation of the atherosclerotic process, significant given atherosclerosis is a disease of the inner intimal layer of the artery, with the media remaining largely intact. Importantly, arterial injury was driven by CSF-1-dependent macrophages (Mφ) accumulating within developing atherosclerotic plaques that exhibited tissue degrading proteolytic activity in vivo. Single-cell RNA sequencing further demonstrated conservation of Mφ responses in atherosclerotic plaque from murine and human AAA. Our findings advance understanding of the pathological sequelae of atherosclerosis, establishing plaque Mφ as important mediators of tissue damage and a potential target for prevention of AAA growth and rupture.
2025-03-06 | GSE284253 | GEO
Project description:There is no effective pharmacotherapy to prevent the growth and rupture of abdominal aortic aneurysms (AAA), a leading cause of death. We developed a novel preclinical model showing that the interaction of bona fide risk factors (i.e., cigarette smoke (CS) and hypercholesterolemia) induced AAA formation, rupture, and death. Elastin fragmentation resulted from CS-induced exacerbation of the atherosclerotic process, significant given atherosclerosis is a disease of the inner intimal layer of the artery, with the media remaining largely intact. Importantly, arterial injury was driven by CSF-1-dependent macrophages (Mφ) accumulating within developing atherosclerotic plaques that exhibited tissue degrading proteolytic activity in vivo. Single-cell RNA sequencing further demonstrated conservation of Mφ responses in atherosclerotic plaque from murine and human AAA. Our findings advance understanding of the pathological sequelae of atherosclerosis, establishing plaque Mφ as important mediators of tissue damage and a potential target for prevention of AAA growth and rupture.
2025-03-06 | GSE284251 | GEO
Project description:There is no effective pharmacotherapy to prevent the growth and rupture of abdominal aortic aneurysms (AAA), a leading cause of death. We developed a novel preclinical model showing that the interaction of bona fide risk factors (i.e., cigarette smoke (CS) and hypercholesterolemia) induced AAA formation, rupture, and death. Elastin fragmentation resulted from CS-induced exacerbation of the atherosclerotic process, significant given atherosclerosis is a disease of the inner intimal layer of the artery, with the media remaining largely intact. Importantly, arterial injury was driven by CSF-1-dependent macrophages (Mφ) accumulating within developing atherosclerotic plaques that exhibited tissue degrading proteolytic activity in vivo. Single-cell RNA sequencing further demonstrated conservation of Mφ responses in atherosclerotic plaque from murine and human AAA. Our findings advance understanding of the pathological sequelae of atherosclerosis, establishing plaque Mφ as important mediators of tissue damage and a potential target for prevention of AAA growth and rupture.
2025-03-06 | GSE284249 | GEO
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: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