Apolipoprotein E derived from CD11c+ cells ameliorates atherosclerosis
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA789533 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:ApoE-/- and Bl6 mice were fed normal chow of high fat diet. CD11c+ cells were isolated from mouse spleens. and mRNA expression was quantified using gene arrays.
2021-12-18 | GSE191044 | GEO
Project description:Atherosclerosis is studied in models with dysfunctional lipid homeostasis-predominantly the ApoE-/- mouse. The role of antigen-presenting cells (APCs) for lipid homeostasis is not clear. Using a LacZ reporter mouse, we showed that CD11c+ cells were enriched in aortae of ApoE-/- mice. Systemic long-term depletion of CD11c+ cells in ApoE-/- mice resulted in significantly increased plaque formation associated with reduced serum ApoE levels. In CD11ccre+ApoEfl/fl and Albumincre+ApoEfl/fl mice, we could show that ≈70% of ApoE is liver-derived and ≈25% originates from CD11c+ cells associated with significantly increased atherosclerotic plaque burden in both strains. Exposure to acLDL promoted cholesterol efflux from CD11c+ cells and cell-specific deletion of ApoE resulted in increased inflammation reflected by increased IL-1β serum levels. Our results determined for the first time the level of ApoE originating from CD11c+ cells and demonstrated that CD11c+ cells ameliorate atherosclerosis by the secretion of ApoE.
| S-EPMC8749187 | biostudies-literature
Project description:Dendritic cells (DCs) are essential for priming of immune responses. Although immune mechanisms are known to control the pathogenesis of atherosclerosis, the role of DCs remains elusive. Here we show that Ccl17 expressing mature, myeloid DCs accumulate within atherosclerotic lesions. Deletion of Ccl17 in apolipoprotein E-deficient (Apoe-/-) mice reduces the development and progression of atherosclerosis in several disease models. While Ccl17 expression by DCs dampened antigen-specific T cell proliferation, it is required for efficient polarization of T helper type 1 (Th1) and Th17 as reflected by a preponderance of Th2 cytokines in Ccl17-/- Apoe-/- mice. In line with these findings, only transfer of T cells from Apoe-/-, but not from Ccl17-/- Apoe-/- precipitated atherosclerosis in T cell depleted Apoe-/- recipients. These findings identify Ccl17+ DCs as central immune regulators in atherosclerosis and Ccl17 as a potential target in the treatment of this disease. There were two samples analyzed with no replicates included. The two samples should be compared with each other.
2011-11-01 | E-GEOD-13642 | biostudies-arrayexpress
Project description:The project was designed to identify genes with an altered expression in macrophages from subjects with atherosclerosis compared to macrophages from control subjects. Experiment Overall Design: We used monocyte-derived macrophages from peripheral blood cultured in the absence or presence of oxidized LDL, baseline macrophages or foam cells. The macrophages were obtained from 15 subjects with subclinical atherosclerosis and a family history of CHD. Macrophages from 15 age and sexmatched subjects with no atherosclerosis and no family history of CHD were used as control.
2008-06-17 | E-GEOD-9874 | biostudies-arrayexpress
Project description:Dendritic cells (DCs) are essential for priming of immune responses. Although immune mechanisms are known to control the pathogenesis of atherosclerosis, the role of DCs remains elusive. Here we show that Ccl17 expressing mature, myeloid DCs accumulate within atherosclerotic lesions. Deletion of Ccl17 in apolipoprotein E-deficient (Apoe-/-) mice reduces the development and progression of atherosclerosis in several disease models. While Ccl17 expression by DCs dampened antigen-specific T cell proliferation, it is required for efficient polarization of T helper type 1 (Th1) and Th17 as reflected by a preponderance of Th2 cytokines in Ccl17-/- Apoe-/- mice. In line with these findings, only transfer of T cells from Apoe-/-, but not from Ccl17-/- Apoe-/- precipitated atherosclerosis in T cell depleted Apoe-/- recipients. These findings identify Ccl17+ DCs as central immune regulators in atherosclerosis and Ccl17 as a potential target in the treatment of this disease. There are three samples analyzed with no replicates included. There is one control sample included.
2011-11-01 | E-GEOD-13592 | biostudies-arrayexpress
Project description:Small extracellular vesicles (sEVs)-derived circular RNAs (circRNAs) could regulate gene expression in recipient cells, and dysregulation of sEVs-derived circRNAs has been implicated in several diseases. However, the expression and function of sEVs-derived circRNAs in coronary atherosclerosis (CAD) remain unknown. In this study, we investigated global changes in the expression patterns of circRNAs in sEVs from coronary atherosclerosis-related monocytes.
2021-10-20 | GSE166126 | GEO
Project description:LARP7 ameliorates cellular senescence and aging-related atherosclerosis by allosterically enhancing SIRT1 deacetylase activity
| PRJNA672873 | ENA
Project description:Cardiovascular diseases, especially atherosclerosis and its complications, are a leading cause of death. Inhibition of the non-canonical IkB kinases TBK1 and IKKe with amlexanox restores insulin sensitivity and glucose homeostasis in diabetic mice and human subjects. Here we report that amlexanox improves diet-induced hypertriglyceridemia and hypercholesterolemia in Western diet (WD)-fed Ldlr-/- mice, and protects against atherogenesis. Amlexanox ameliorates dyslipidemia, inflammation and vascular dysfunction through synergistic actions that involve upregulation of bile acid synthesis to increase cholesterol excretion. Transcriptomic profiling demonstrates an elevated expression of key bile acid synthesis genes. Furthermore, we found that amlexanox attenuates monocytosis, eosinophilia and vascular dysfunction during WD-induced atherosclerosis. These findings demonstrate the potential of amlexanox as a new therapy for hypercholesterolemia and atherosclerosis.
2022-07-27 | GSE209621 | GEO
Project description:We applied Illumina massively parallel signature sequencing to identify miRNomes in CD11c+Ia high and CD11c+Ia low cells.The miRNomes of these DC subsets will contribute to investigate the significance of miRNAs in DC immunobiology. Examination of miRNome in CD11c+Ia high and CD11c+Ia low cells . All two mouse cell types.
2015-06-16 | E-GEOD-51574 | biostudies-arrayexpress
Project description:We cultured bone marrow derived dendritic cells from WT and CD11c KO mice. Then, a group of bone marrow dendritic cells were stimulated with LPS overnight. We obtained bone marrow derived dendritic cells with or without LPS stimulation and analyzed proteomics profiles.
2024-01-26 | PXD048907 | iProX