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

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

PROVIDER: PRJNA835106 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19086625.fastq.gz	Fastqsanger.gz
	SRR19086626.fastq.gz	Fastqsanger.gz
	SRR19086627.fastq.gz	Fastqsanger.gz
	SRR19086628.fastq.gz	Fastqsanger.gz
	SRR19086629.fastq.gz	Fastqsanger.gz

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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

Lack of ApoA-I in ApoEKO Mice Causes Skin Xanthomas, Worsening of Inflammation, and Increased Coronary Atherosclerosis in the Absence of Hyperlipidemia.

Project description:BackgroundHDL (high-density lipoprotein) and its major protein component, apoA-I (apolipoprotein A-I), play a unique role in cholesterol homeostasis and immunity. ApoA-I deficiency in hyperlipidemic, atheroprone mice was shown to drive cholesterol accumulation and inflammatory cell activation/proliferation. The present study was aimed at investigating the impact of apoA-I deficiency on lipid deposition and local/systemic inflammation in normolipidemic conditions.MethodsApoE deficient mice, apoE/apoA-I double deficient (DKO) mice, DKO mice overexpressing human apoA-I, and C57Bl/6J control mice were fed normal laboratory diet until 30 weeks of age. Plasma lipids were quantified, atherosclerosis development at the aortic sinus and coronary arteries was measured, skin ultrastructure was evaluated by electron microscopy. Blood and lymphoid organs were characterized through histological, immunocytofluorimetric, and whole transcriptome analyses.ResultsDKO were characterized by almost complete HDL deficiency and by plasma total cholesterol levels comparable to control mice. Only DKO showed xanthoma formation and severe inflammation in the skin-draining lymph nodes, whose transcriptome analysis revealed a dramatic impairment in energy metabolism and fatty acid oxidation pathways. An increased presence of CD4+ T effector memory cells was detected in blood, spleen, and skin-draining lymph nodes of DKO. A worsening of atherosclerosis at the aortic sinus and coronary arteries was also observed in DKO versus apoE deficient. Human apoA-I overexpression in the DKO background was able to rescue the skin phenotype and halt atherosclerosis development.ConclusionsHDL deficiency, in the absence of hyperlipidemia, is associated with severe alterations of skin morphology, aortic and coronary atherosclerosis, local and systemic inflammation.

| S-EPMC9205301 | biostudies-literature

The apoA-I induced transcriptome and dependence on MyD88

Project description:Apolipoprotein A-I is well known to play a role in cholesterol efflux, but our studies suggest that apoA-I may also induce proinflammatory signaling. The molecular mechanisms behind apoA-I-mediated proinflammatory signaling have not yet been explored, nor has the link between this signaling and cholesterol efflux. We hypothesize that apoA-I is a novel TLR agonist, signaling through the MyD88 proinflammatory signaling adaptor to induce cytokines. Microarray analysis confirmed that a suite of pro-inflammatory genes are induced by apoA-I with varying dependence upon MyD88, and that MyD88 regulates >6% of the apoA-I-induced transcriptome.

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Genetic Copy Number Variants in Myocardial Infarction Patients with Hyperlipidemia

Project description:We identified 7 CNV regions that were associated significantly with hyperlipidemia and myocardial infarction in our patients through multistage analysis (P<0.001). The inclusion criteria for enrolling patients were drawn from the Prospective Cardiovascular Munster study [http://www.ncbi.nlm.nih.gov/pubmed/3202078] and Framingham Heart Study [http://www.ncbi.nlm.nih.gov/pubmed/9737513]. In brief, patients aged between 20 and 75 years with coronary arterial disease with more than 50% stenosis, as proven by cardiac catheterization, and a history of hyperlipidemia with serum cholesterol level greater than 240 mg/dL or low-density lipoprotein greater than 155 mg/dL were enrolled.

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Genetic Copy Number Variants in Myocardial Infarction Patients with Hyperlipidemia

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Bulk RNA-seq of primary microglia with LPS stress and ApoA-I treatment

Project description:To test the functional role of ApoA-I on microglia in the context of stress, we treated primary microglia with LPS stress with or without ApoA-I protein, and used bulk RNA-seq to evaluate if ApoA-I exhibits an anti-inflammatory role.

2024-10-15 | GSE264110 | GEO

Bulk RNA-seq of microglia from Apoa1 KO mice injected with ApoA-I protein intravenously

Project description:We found ApoA-I from blood can be taken up by microglia in the brain. To determine if ApoA-I from circulation is sufficient to restore microglial transcriptomic state to a more wild-type-like state, we performed a rescue experiment by intravenously injecting ApoA-I protein into adult Apoa1 KO mice and sorted microglia with or without ApoA-I uptake for bulk transcriptomic analysis.

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Hyperlipidemia elicits an IFN-based CD4+ T cell response

Project description:Hyperlipidemia is accompanied by increased systemic inflammation. However, how hyperlipidemia affects T cell biology is still unclear. We aimed to detail the effects of hyperlipidemia on the T cell’s transcriptome, metabolome and lipidome. Low-density lipoprotein receptor-deficient (LDLR-/-) mice were subjected to a 0.15% high cholesterol diet (HCD), a normal chow diet (NCD) and T cells were analyzed. Hyperlipidemia induced an increase in CXCR3 on and IFN in CD4+ T cells, which was accompanied by transcriptomic changes in interleukin-mediated JAK/STAT signaling, interferon-γ signaling and a general pro-inflammatory immune response, suggesting that hyperlipidemia induces a Th1-like response. In these T cells, hyperlipidemia did not affect levels of metabolites involved in glycolysis or fatty acid oxidation, but enhanced amino acids levels. CD4+ T-cells of mice fed a HCD exhibited increased cellular cholesterol accumulation and an increased arachidonic acid (AA) to Docosahexaenoic acid (DHA) ratio, which was associated with T cell activation and IFN signaling. In vitro, T cell exposure to VLDL, but not LDL phenocopied these results. The effect of hyperlipidemia on T cell activation is reversible as transcriptional- and lipid profiles in LDLr-/ mice normalized 6 weeks after switching the HCD to NCD. In conclusion, hyperlipidemia induces a Th1-like response in CD4+ T cells, which is associated with an AA/DHA ratio in these cells. VLDL, but not LDL is the main lipid component driving hyperlipidemia induced T cell activation.

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ApoA-1 and Atherosclerosis in Psoriasis

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