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

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

PROVIDER: PRJNA687012 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13320444.fastq.gz	Fastqsanger.gz
	SRR13320445.fastq.gz	Fastqsanger.gz
	SRR13320446.fastq.gz	Fastqsanger.gz
	SRR13320447.fastq.gz	Fastqsanger.gz
	SRR13320448.fastq.gz	Fastqsanger.gz

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Similar Datasets

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

Aortic Gene Expression Profiles Show How ApoA-I Levels Modulate Inflammation, Lysosomal Activity, and Sphingolipid Metabolism in Murine Atherosclerosis.

Project description:ObjectiveHDL (high-density lipoprotein) particles are known to possess several antiatherogenic properties that include the removal of excess cholesterol from peripheral tissues, the maintenance of endothelial integrity, antioxidant, and anti-inflammatory 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. Approach and Results: Eight-week-old EKO mice, EKO mice overexpressing human apoA-I, and wild-type mice as controls were fed either normal laboratory 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 analyze the transcriptome of the aorta of the 3 genotypes in each experimental condition. 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 immune system markers, as well as reduced perturbation of lysosomal activity and a better regulation of the sphingolipid synthesis pathway.ConclusionsApoA-I modulates atherosclerosis development in the aorta of EKO mice affecting the expression of pathways additional to those associated with inflammation and immune response.

| S-EPMC7837693 | biostudies-literature

ApoA-1 and Atherosclerosis in Psoriasis

Project description:ApoA-1 and Atherosclerosis in Psoriasis

| PRJNA946881 | ENA

ApoA-1 and Atherosclerosis in Psoriasis

Project description:ApoA-1 and Atherosclerosis in Psoriasis

| PRJNA946882 | ENA

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.

2010-06-15 | GSE13772 | GEO

A lysosome-plasma membrane-sphingolipid axis linking lysosomal storage to cell growth arrest

Project description:A lysosome-plasma membrane-sphingolipid axis linking lysosomal storage to cell growth arrest

| PRJNA418450 | ENA

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

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.

2024-10-15 | GSE264111 | GEO

Inhibiting sphingolipid synthesis improves outcomes and survival in GARP-mutant wobbler mouse, an ALS model

Project description:Defects of the endosomal and lysosomal systems have been increasingly linked to adult neurodegenerative diseases1,2. Deficiencies in the retrograde trafficking pathway between endosomes and the Golgi apparatus lead to forms of Alzheimer’s and Parkinson’s diseases in the case of retromer mutations, or to the rare progressive cerebello-cerebral atrophy type 2 (PCCA2) for mutations of the Golgi-associated retrograde protein (GARP) complex3. Mutations in GARP subunits lead to abnormal cellular lipid metabolism, with accumulation of sterol esters and sphingoid bases, and concomitant lysosomal dysfunction in yeast, murine, or human cells4,5. However, whether these lipid changes cause neurodegeneration and if so, which lipids are toxic, is unknown. Here, we show that GARP defects lead to global changes of cellular protein distribution, including missorting of numerous disease-linked enzymes of sphingolipid metabolism, and to the accumulation of sphingolipid intermediates in wobbler fibroblasts. Inhibiting sphingolipid synthesis in wobbler mice, a murine model of GARP deficiency with features of amyotrophic lateral sclerosis (ALS), improved wellness scores and grip strength, and increased lifespan. Our findings indicate that regulation of sphingolipids by the GARP complex is essential for neuronal health and suggest that inhibition of sphingolipid synthesis might provide a therapeutic strategy for treatment of neurodegenerative diseases due to defects in retrograde endosome-to-Golgi membrane trafficking.

2022-02-15 | PXD007981 | Pride

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