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A Western Dietary Pattern and Atorvastatin Induce Epicardial Adipose Tissue Interferon Signaling in the Ossabaw Pig

ABSTRACT: A Western Dietary Pattern and Atorvastatin Induce Epicardial Adipose Tissue Interferon Signaling in the Ossabaw Pig

PROVIDER: PRJNA530773 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8844240.fastq.gz	Fastqsanger.gz
	SRR8844250.fastq.gz	Fastqsanger.gz
	SRR8844260.fastq.gz	Fastqsanger.gz
	SRR8844241.fastq.gz	Fastqsanger.gz
	SRR8844251.fastq.gz	Fastqsanger.gz

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A Western Dietary Pattern and Atorvastatin Induce Epicardial Adipose Tissue Interferon Signaling in the Ossabaw Pig

2020-02-04 | GSE129301 | GEO

Colon Transcriptome is Modified by a Dietary Pattern/Atorvastatin Interaction in the Ossabaw Pig

Project description:Colon Transcriptome is Modified by a Dietary Pattern/Atorvastatin Interaction in the Ossabaw Pig

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A Western-type dietary pattern and atorvastatin induce epicardial adipose tissue interferon signaling in the Ossabaw pig.

Project description:Epicardial adipose tissue (EAT) inflammation is thought to potentiate the development of coronary artery disease (CAD). Overall diet quality and statin therapy are important modulators of inflammation and CAD progression. Our objective was to examine the effects and interaction of dietary patterns and statin therapy on EAT gene expression in the Ossabaw pig. Pigs were randomized to 1 of 4 groups; Heart Healthy diet (high in unsaturated fat, unrefined grain, fruits/vegetables [HHD]) or Western diet (high in saturated fat, cholesterol, refined grain [WD]), with or without atorvastatin. Diets were fed in isocaloric amounts for 6 months. A two-factor edge R analysis identified the differential expression of 21 genes. Relative to the HHD, the WD resulted in a significant 12-fold increase of radical s-adenosyl methionine domain containing 2 (RSAD2), a gene induced by interferon signaling. Atorvastatin led to the significant differential expression of 17 genes predominately involved in interferon signaling. Results were similar using the Porcine Translational Research Database. Pathway analysis confirmed the up-regulation of interferon signaling in response to the WD and atorvastatin independently. An expression signature of the largely interferon related differentially expressed genes had no predictive capability on a histological assessment of atherosclerosis in the underlying coronary artery. These results suggest that a WD and atorvastatin evoke an interferon mediated immune response in EAT of the Ossabaw pig, which is not associated with the presence of atherosclerosis.

| S-EPMC6935368 | biostudies-literature

Colon Transcriptome is Modified by a Dietary Pattern/Atorvastatin Interaction in the Ossabaw Pig

Project description:Overall diet quality and statin therapy are important modulators of inflammation and CAD progression, yet their effects on colon is not well understood. Our objective was to examine the effects and interaction of dietary patterns and statin therapy on colonic mucosa gene expression in the Ossabaw pig.

2021-12-30 | GSE163159 | GEO

A Western-type Dietary Pattern Induces an Atherogenic Gene Expression Profile in the Coronary Arteries of the Ossabaw Pig

Project description:We investigated the effect of 2 food-based dietary patterns and statin therapy on the transcriptome of the left anterior descending coronary artery of the Ossabaw pig.

2019-05-09 | GSE129300 | GEO

Gene expression profiles in HepG2 cells exposed to atorvastatin

Project description:In the exon array data set, gene level analysis was performed on HepG2 cells exposed to atorvastatin. No genes were found to be statistically significantly differentially expressed upon atorvastatin treatment.

2014-04-26 | GSE57071 | GEO

A Western-type Dietary Pattern Induces an Atherogenic Gene Expression Profile in the Coronary Arteries of the Ossabaw Pig

Project description:A Western-type Dietary Pattern Induces an Atherogenic Gene Expression Profile in the Coronary Arteries of the Ossabaw Pig

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Endothelial cells and atorvastatin

Project description:Rationale: Immortalized cells may exhibit important differences relative to their primary cell counterparts. Microarrays were used compare primary human umbilical vein endothelial cells (HUVECs) and the immortalized HUVEC cell line EA.hy926, in their response to inhibition of the mevalonate pathway by a HMG-CoA reductase inhibitor (atorvastatin). The effects of atorvastatin were reversed by the addition of mevalonate, to subtract non-specific changes in gene expression. Methods: Confluent cell cultures of HUVECs and EA.hy926 cells (two independent experiments in each cell type) were incubated with 1) statin-free media; 2) 10 microM atorvastatin; 3) 500 microM mevalonate; or 4) a combination of 10 microM atorvastatin and 500 microM mevalonate. All cells were harvested at 24 h. Total RNA was isolated using Trizol reagent (Invitrogen). cDNA was prepared from 10 microgram total RNA using a double-stranded cDNA synthesis kit (Life Technologies) with a T7-dT24 primer for first-strand synthesis. cRNA was synthesized from cDNA and biotinylated using the BioArray High Yield RNA Transcript Labeling Kit (Enzo Diagnostics). Twenty microgram of cRNA was fragmented by heating at 94°C for 35 min in fragmentation buffer, containing 40 mM Tris-acetate, pH 8.1, 125 mM KOAc, 30 mM MgOAc. Fifteen micrgram of fragmented cRNA, together with control cRNAs and grid alignment oligonucleotides, were hybridized overnight to GeneChip Human Genome U133A 2.0 arrays (Affymetrix) at 45°C under constant rotation. Arrays were washed and incubated with an anti-streptavidin antibody. Fluorescent signals were measured using an Agilent Gene Array Laser Scanner and analyzed with MicroArray Suite 5.0 (Affymetrix). Microarrays were scaled using default settings. Keywords: other

2005-03-29 | GSE2450 | GEO

Atorvastatin improved ulcerative colitis in association with gut microbiota-derived tryptophan metabolism

Project description:Aims: Atorvastatin is a commonly used cholesterol-lowering drug that possesses non-canonical anti-inflammatory properties. However, the precise mechanism underlying its anti-inflammatory effects remains unclear. Materials and methods: The acute phase of ulcerative colitis (UC) was induced using a 5 % dextran sulfate sodium (DSS) solution for 7 consecutive days and administrated with atorvastatin (10 mg/kg) from day 3 to day 7. mRNA-seq, histological pathology, and inflammatory response were determined. Intestinal microbiota alteration, tryptophan, and its metabolites were analyzed through 16S rRNA sequencing and untargeted metabolomics. Key findings: Atorvastatin relieved the DSS-induced UC in mice, as evidenced by colon length, body weight, disease activity index score and pathological staining. Atorvastatin treatment reduced the level of pro_x0002_inflammatory cytokines interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α). Atorvastatin also relieved the intestinal microbiota disorder caused by UC and decreased the proliferation of pernicious microbiota such as Akkermansia and Bacteroides. Atorvastatin dramatically altered tryptophan metabolism and increased the fecal contents of tryptophan, indolelactic acid (ILA), and indole-3-acetic acid (IAA). Furthermore, atorvastatin enhanced the expression level of aryl hydrocarbon receptor (AhR) and interleukin-22 (IL-22) and further promoted the expression level of intestinal tight junction proteins, such as ZO-1 and occludin, in colitis mice. Significance: These findings indicated that atorvastatin could alleviate UC by regulating intestinal flora disorders, promoting microbial tryptophan metabolism, and repairing the intestinal barrier.

2024-11-04 | GSE280960 | GEO

CDH18 is an epicardial biomarker regulating epicardial specification and differentiation towards vascular smooth muscle cells

Project description:The epicardium is a mesothelial layer covering the myocardium and contributes to different cardiac lineage descendants during cardiogenesis. Fine-tuned balanced signaling defines epicardial specification and regulates cell plasticity and cell-fate decisions of epicardial-derived cells (EPCDs) by epicardial-to-mesenchymal transition (EMT). However, powerful tools to investigate epicardial cell function, including markers with pivotal roles in developmental signaling, are still lacking. Here, we recapitulated embryonic epicardiogenesis using human induced pluripotent stem cells (hiPSCs) and identified type II classical cadherin CDH18 as a novel biomarker defining lineage specification in human developing epicardium. The loss of CDH18 led to the onset of EMT and specific differentiation towards cardiac smooth muscle cells. Furthermore, GATA4 regulated epicardial CDH18 expression. These results demonstrate the production and enrichment of hiPSC-derived epicardial cells via the tracing of CDH18 expression, providing a model for investigating epicardial function in human development and disease and enabling new possibilities for regenerative medicine.

2022-02-18 | GSE165450 | GEO

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