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Aortic gene expression profiles of double ApoE and ApoA-I knockout mice

ABSTRACT: Eight weeks old double apolipoprotein E and apolipoprotein A-I knockout mice (DKO) were fed either normal laboratory diet (chow) or high-fat (Western) diet for 6 or 22 weeks. High-throughput sequencing technologies were used to analyse the transcriptome of the aorta of apolipoprotein E knockout (EKO, GSE163657) and DKO mice to showcase the use of the software reString (https://github.com/Stemanz/restring), a functional enrichment results aggregator.

ORGANISM(S): Mus musculus

PROVIDER: GSE173974 | GEO | 2021/11/22

REPOSITORIES: GEO

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Aortic gene expression profiles show how APOA-I levels modulate infammation, lysosomal activity and sphingolipid metabolism in murine atherosclerosis

Project description:HDL particles are known to possess several anti-atherogenic properties that include the removal of excess cholesterol from peripheral tissues, the maintenance of endothelial integrity, antioxidant and antiinflammatory activities. ApoA-I overexpression in apoE-deficient (EKO) mice has been shown to increase HDL levels and to strongly reduce atherosclerosis development. The aim of the study was to investigate gene expression patterns associated with atherosclerosis development in the aorta of EKO mice and how HDL plasma levels relate to gene expression patterns at different stages of atherosclerosis development and with different dietary treatments. Methods Eight weeks old EKO mice, EKO mice overexpressing human apoA-I (EKO/hA-I) and wild-type mice as controls were fed either Chow or Western diet for 6 or 22 weeks. Cholesterol distribution among lipoproteins was evaluated and atherosclerosis of the aorta was quantified. High-throughput sequencing technologies were used to analyse the transcriptome of the aorta of the three genotypes in each experimental condition. Results: In addition to the well-known activation of inflammation and immune response, the impairment of sphingolipid metabolism, phagosome-lysosome system and osteoclast differentiation emerged as relevant players in atherosclerosis development. The reduced atherosclerotic burden in the aorta of EKO mice expressing high levels of apoA-I was accompanied by a reduced activation of the immune system markers, as well as reduced perturbation of lysosomal activity and a better regulation of the sphingolipid synthesis pathway Conclusions. ApoA-I modulates atherosclerosis development in the aorta of EKO mice affecting the expression of pathways additional to those associated with inflammation and immune response

2020-12-22 | GSE163657 | GEO

Expression data from the aortas of ApoE knockout, ApoE/Caspase-1 double knockout, and wild-type mice

Project description:Caspase-1 activation senses metabolic danger-associated molecular patterns and mediates the initiation of inflammation. Here, we reported that caspase-1 contributes to hyperlipidemia-induced modulation of vascular cell gene expression during early atherosclerosis in vivo. Our results demonstrate the therapeutic potential of caspase-1 inhibition in the treatment of cardiovascular diseases. All mice were in a C57B/L6 strain background. Male wild-type mice, Apolipoprotein E (ApoE) gene knockout mice, and ApoE/Caspase-1 double gene deficient mice were fed with high fat diet for 3 weeks starting from 8 weeks to induce early dyslipidemia. At 11-week of age, aortas from these mice were used for microarray analysis. 5 biological replicates in each group.

2015-08-21 | E-GEOD-72248 | biostudies-arrayexpress

Lack of apoA-I in apoEKO mice causes skin xanthomas, worsening of inflammation and increased coronary atherosclerosis in the absence of hyperlipidemia

Project description:High-throughput sequencing technologies were used to analyse the transcriptome of the spleen and axillary lymph node of apoE/apoA-I double deficient (DKO) mice, characterized by an almost complete HDL deficiency, and DKO mice overexpressing human apoA-I (DKO/hA-I), characterized by high HDL plasma levels. Mice were 30 weeks old and had been fed a normal laboratory diet.

2022-05-07 | GSE202237 | GEO

Expression data from ADORA1 knockout and ADORA1 APOE double-knockout mice

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

ApoE-knockout mice liver on high fat diet treated with trehalose or agmatine.

Project description:ApoE-knockout mice liver on high fat diet developing liver steatosis were treated with trehalose or agmatine for 16 weeks.

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Transcriptome profiling of murine aortic Vascular Smooth Muscle cells from ApoE knockout and ApoE/Neil3 double knockout mice

Project description:We performed high-throughput RNA sequencing to characterize possible differences in the transcriptome of murine aortic Vascular Smooth Muscle cells from both 26 weeks-old ApoE knockout and ApoE/Neil3 double knockout mice fed a regular diet.

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Sex differences in statin response in hypercholesterolemic (Apoe knockout) Four Core Genotypes mice.

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Gene expression from epidydimal fat pad

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2013-12-01 | E-GEOD-44653 | biostudies-arrayexpress

Effect of ApoE in communicating immunometabolic signaling in recipient macrophages via exosomes

Project description:While ApoE expression by myeloid cells is recognized to control inflammation, whether such benefits can be communicated via extracellular vesicles including exosomes is not known. Through the study of exosomes produced by macrophages derived from the bone marrow of Wildtype (WT-BMDM-exo) and ApoE deficient (EKO-BMDM-exo) mice, we uncover a critical role of ApoE in regulating cell signaling properties. We treated BMDM with EKO-BMDM-exo, WT-BMDM-exo, or PBS and performed gene expression profiling analysis. We found that BMDM treated with EKO-BMDM-exo show reductions in the cholesterol efflux gene Abca1 and the long chain fatty acid transporter Cpt1a. Furthermore, BMDM treated with EKO-BMDM-exo show reduced expressions of genes involved in oxidative stress response, particularly the glutathione peroxidases (Gpx1 & Gpx3) and the selenoproteins (Selenow, Selenom, Selenop, and Selenon). In contrast, treatments of these EKO-BMDM-exo upregulated the expressions of genes reported to drive glycolysis or involved in the glycolytic pathway (Aldh2, Pkm, Cd9, Fth1, Dio2, and Pgd). Taken together, our data unveil a novel property of macrophage ApoE in controlling the immunometabolism-regulatory properties by their secreted exosomes.

2024-07-18 | GSE237730 | GEO

Expression data from browning inguinal white adipose tissue in UCP1/ApoE-DKO mice

Project description:Differentiation of brown adipocytes is a crucial process for adaptive thermogenesis, which is stimulated by various factors. We found robust browning of inguinal white adipose tissue in UCP1/ApoE-DKO mice, but not in ApoE-KO mice, under high-fat diet condition. We used microarray to determine the genes specifically regulated in the browning white adipose tissue in UCP1/ApoE-DKO mice.

2018-10-01 | GSE95273 | GEO

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