Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA184759 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Aortic macrophages and endothelial cells of apoE KO mice were sorted and analyzed by microarray 2 weeks after regression was induced by adenoviral transfer of apoE. Aortic macrophages (CD45+ F4/80+ CD11b+) and endothelial cells (CD45- CD31+) were sorted from apoE KO mice and the RNA extracted and hybridized to Affymetrix Mouse Gene 1.0 ST array. We pooled aortas from 5 mice for each sort.
2015-01-01 | E-GEOD-42691 | biostudies-arrayexpress
Project description:Aortic macrophages and endothelial cells of apoE KO mice were sorted and analyzed by microarray 2 weeks after regression was induced by adenoviral transfer of apoE.
2015-01-01 | GSE42691 | GEO
Project description:Objective—Overexpression or administration of sclerostin has been reported to have atheroprotective and anti-inflammatory effects in apolipoprotein E knockout (ApoE KO) mice infused with angiotensin II; however, effects of sclerostin inhibition on these processes are not known. This study examined the effects of sclerostin inhibition with a sclerostin antibody on transcriptional changes in the aortic arch, associated morphological changes in aortic atherosclerotic plaques, and circulating markers of inflammation in ApoE KO ovariectomized (OVX) mice fed a high-fat diet. Approach and Results—Sclerostin antibody or vehicle was administered by subcutaneous injection once weekly for 3, 8, or 16 weeks to ApoE KO-OVX and wild-type-OVX mice fed a high-fat diet. As a comparator, alendronate or saline was administered twice weekly for 16 weeks to ApoE KO-OVX mice fed a high-fat diet. Sclerostin antibody had no effect on aortic total or mineralized plaque volume, determined by microcomputed tomography. Sclerostin antibody had no meaningful effects on plaque histopathology or systemic markers of inflammation or endothelial/platelet activation. Transcriptional analysis of the aortic arch revealed significant gene expression and signaling pathway changes in ApoE KO mice compared with wild-type, consistent with the genotype and atheroprogression, that were not affected by sclerostin antibody treatment. Alendronate treatment did not alter plaque volume or histopathology. Conclusions—This study shows that inhibition of sclerostin by sclerostin antibody does not promote atheroprogression or affect systemic markers of inflammation in the high-fat diet ApoE KO-OVX mouse model and does not alter the expression of genes/pathways implicated in atherosclerosis.
2020-05-01 | GSE130995 | GEO
Project description:The goal of this study is to determine whether A1 adenosine receptor (ADORA1) plays a role in atherosclerosis development and its possible mechanisms. This dataset compares gene expression (aortas) of ADORA1 knockout mice to ADORA1+APOE double-knockout mice. Mice deficient in both ADORA1 and APOE (DKO) demonstrated reduced atherosclerotic lesions in aortic arch (en face), aortic root, and innominate arteries when compared to (APOE-KO) of the same age. Treating APOE-KO with the ADORA1 antagonist DPCPX also achieved concentration-dependent reduction in lesions. The total plasma cholesterol and triglyceride levels were not different between DKO and APOE-KO, however, higher triglyceride was observed in DKO fed a high-fat diet. DKO also were heavier than APOE-KO. Plasma cytokine levels (IL-5, IL-6, and IL-13) were significantly lower in DKO. Proliferating cell nuclear antigen (PCNA) expression was also significantly reduced in the aorta from DKO. Despite smaller lesions in DKO, the composition of the innominate artery lesions and cholesterol loading and effusion [export] from bone-marrow-derived macrophages from DKO were not different from APOE-KO.
2015-06-02 | GSE39888 | GEO
Project description:This study compared gene expression in smooth muscle cells (SMCs) in atherosclerosis-prone and atherosclerosis-resistant aorta segments in 4 months old apolipoprotein E-deficient (apoE-/-) mice before plaque development. In a parallel experiment, both regions were compared in young C57Bl/6 mice. Aortas of 3 male and 3 female ApoE-/- mice were isolated, perfused with triton X-100 to remove endothelial cells and divided in an atherosclerosis-prone region (AA: ascending aorta, aortic arch and proximal 2 mm of thoracic aorta) and a resistant region (TA: central thoracic aorta, i.e. 6 mm distal from the proximal 2 mm). Microarray analysis (VIB-MAF) of pooled total RNA showed differential expression (>2-fold difference) for 244 genes. Up- or downregulation in the AA was observed for 186 and 58 genes respectively. Differential expression of 6 genes was confirmed using real-time PCR. The 201 genes that showed exclusively differential expression in apoE-/- mice were related to processes involved in atherosclerosis, such as cell adhesion, proliferation, differentiation, motility and death, lipid metabolism and immune responses. Furthermore, the transcription profile of the AA was in accordance with a more synthetic SMC phenotype. These results point to an altered transcriptome in SMCs in the aorta of apoE-/- mice at the atherosclerosis-prone location before actual lesion development. This suggests that SMCs, in addition to endothelial cells, can facilitate plaque formation at predilection sites. Experiment Overall Design: samples were hyrbidized in dye-swap.
2009-05-27 | E-GEOD-13836 | biostudies-arrayexpress
Project description:In atherosclerosis progression and regression, monocytes or monocyte-derived macrophages are the major immune cells in the plaque. It is important to understand the fate and characteristics of monocyte/macrophage during the plaque progression and regression. To characterize the fate of monocytes/macrophages, we performed single cell RNA sequencing of fate-mapped aortic CX3CR1-derived monocytes/macrophages from Cx3cr1CreERT2-IRES-YFP/+Rosa26floxed-tdTomato/+ mice with AAV-PCSK9 injection and fed a Western Diet. The single cell RNA-seq analyses revealed the heterogeneity of aortic macrophages and identified a stem-like cell cluster in atherosclerotic aorta.
2019-02-21 | GSE123587 | GEO
Project description:Atherosclerosis is the leading underlying cause of death worldwide. We reported a mouse model of atherosclerosis regression that involves transplanting an atherosclerotic aortic arch into a normolipidemic mouse. There, emigration of plaque foam cells occurred in a CCR7 (dendritic cell migration factor) dependent manner. It was obvious, though, that other pathways are likely to be involved in this process. We therefore performed microarrays on laser captured macrophages isolated from the progression and regression environments. This yielded two major findings. Firstly, genes associated with the contractile apparatus (such as actin and myosin) that are responsible for cellular movement were differentially up-regulated under regression conditions with members of the cadherin family (serves in adhesion functions) being significantly down-regulated. Secondly, the most highly up-regulated gene under regression was arginase I, a classical marker of the M2 alternative activated macrophage. Further examination revealed that regression was characterized by macrophages displaying other M2 markers such as CD163, C-lectin receptor, mannose receptor, and Fizz-1. In addition, we applied recently introduced local causal pathway discovery methods to our microarray data that revealed that genes such as vinculin and ApoCII may play a role in the pathophysiology of atherosclerosis regression. Ultimately, the insights gained from the regression model and the different modes of analyses should lead to new therapeutic targets against cardiovascular disease. We performed microarrays on laser captured macrophages isolated from aortic arch from mouse in atherosclerosis progression and regression environments (C57Bl/6, ApoE -/-). Study was performed in two batches, with three treatment groups each: progression, regression and baseline. Profiled in the Merck/Agilent 3.0
2011-09-30 | E-GEOD-24819 | biostudies-arrayexpress
Project description:Peripherally restricted cannabinoid CB1 receptor antagonists without central side effects hold promise for treating metabolic disorders including diabetes and obesity. In atherosclerosis, the specific effects of peripheral CB1 signaling in vascular endothelial cells (ECs) remain incompletely understood.We performed en face in situ hybridization of Cnr1 in murine aortas, revealing a significantly increased expression of the CB1 encoding gene in ECs within atheroprone compared to atheroresistant regions. In vitro, CNR1 was upregulated by oscillatory shear stress in human aortic endothelial cells (HAoECs). Endothelial CB1 deficiency (Cnr1EC-KO) in female mice on atherogenic background resulted in pronounced endothelial phenotypic changes, with reduced vascular inflammation and permeability. This translated into attenuated plaque development with reduced lipid content as well as reduced white and brown adipose tissue mass and liver steatosis. Ex vivo imaging of carotid arteries via two-photon microscopy revealed less DIL-LDL uptake in Cnr1EC-KO. This was accompanied by a significant reduction of aortic endothelial caveolin-1 (CAV1) expression, a key structural protein involved in lipid transcytosis in female Cnr1EC-KO mice. In vitro, pharmacological blocking with CB1 antagonist AM281 reproduced the inhibition of CAV1 expression and LDL uptake in response to atheroprone shear stress in human aortic endothelial cells (HAoECs), which was dependent on cAMP-mediated PKA activation. Conversely, the CB1 agonist ACEA increased DIL-LDL uptake and CAV1 expression in HAoECs. Finally, treatment of atherosclerotic mice with the peripheral CB1 antagonist JD-5037 reduced plaque progression, CAV1 and endothelial adhesion molecule expression in female mice. These results confirm an essential role of endothelial CB1 to the pathogenesis of atherosclerosis.
2024-04-04 | GSE260826 | GEO
Project description:Transcriptional profiling of aortic sinus atherosclerotic plaque macrophages obtained by laser capture microdissection from male ApoE deficient mice infected with 5x10(5) cfu serotype 4 Streptococcus pneumoniae via intranasal instillation (n=9) as compared with mice mock infected with PBS (n=11). Mice were culled 2 weeks post infection/mock infection.
2022-02-15 | E-MTAB-11462 | biostudies-arrayexpress
Project description:This study compared gene expression in smooth muscle cells (SMCs) in atherosclerosis-prone and atherosclerosis-resistant aorta segments in 4 months old apolipoprotein E-deficient (apoE-/-) mice before plaque development. In a parallel experiment, both regions were compared in young C57Bl/6 mice. Aortas of 3 male and 3 female ApoE-/- mice were isolated, perfused with triton X-100 to remove endothelial cells and divided in an atherosclerosis-prone region (AA: ascending aorta, aortic arch and proximal 2 mm of thoracic aorta) and a resistant region (TA: central thoracic aorta, i.e. 6 mm distal from the proximal 2 mm). Microarray analysis (VIB-MAF) of pooled total RNA showed differential expression (>2-fold difference) for 244 genes. Up- or downregulation in the AA was observed for 186 and 58 genes respectively. Differential expression of 6 genes was confirmed using real-time PCR. The 201 genes that showed exclusively differential expression in apoE-/- mice were related to processes involved in atherosclerosis, such as cell adhesion, proliferation, differentiation, motility and death, lipid metabolism and immune responses. Furthermore, the transcription profile of the AA was in accordance with a more synthetic SMC phenotype. These results point to an altered transcriptome in SMCs in the aorta of apoE-/- mice at the atherosclerosis-prone location before actual lesion development. This suggests that SMCs, in addition to endothelial cells, can facilitate plaque formation at predilection sites.
2009-05-15 | GSE13836 | GEO