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Directed Remodeling of the Mouse Gut Microbiome Inhibits the Development of Atherosclerosis

ABSTRACT: Directed Remodeling of the Mouse Gut Microbiome Inhibits the Development of Atherosclerosis

PROVIDER: PRJNA414124 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6166340.fastq.gz	Fastqsanger.gz
	SRR6166350.fastq.gz	Fastqsanger.gz
	SRR6166360_1.fastq.gz	Fastqsanger.gz
	SRR6166360_2.fastq.gz	Fastqsanger.gz
	SRR6166341.fastq.gz	Fastqsanger.gz

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Directed Remodeling of the Mouse Gut Microbiome Inhibits the Development of Atherosclerosis [bacteria]

Project description:Directed Remodeling of the Mouse Gut Microbiome Inhibits the Development of Atherosclerosis [bacteria]

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Directed Remodeling of the Mouse Gut Microbiome Inhibits the Development of Atherosclerosis [mouse tissue]

Project description:Directed Remodeling of the Mouse Gut Microbiome Inhibits the Development of Atherosclerosis [mouse tissue]

| PRJNA414149 | ENA

Directed Remodeling of the Mouse Gut Microbiome Inhibits the Development of Atherosclerosis [bacteria]

Project description:The gut microbiome is a malleable microbial community that can remodel in response to various factors, including diet, and contribute to the development of several chronic diseases, including atherosclerosis. We devised an in vitro screening protocol of the mouse gut microbiome to discover molecules that can selectively modify bacterial growth. This approach was used to identify cyclic D,L-α-peptides that remodeled the Western diet (WD) gut microbiome toward the low-fat-diet microbiome state. Daily oral administration of the peptides in WD-fed LDLr-/- mice reduced plasma total cholesterol levels and atherosclerotic plaques. Depletion of the microbiome with antibiotics abrogated these effects. Peptide treatment reprogrammed the microbiome transcriptome, suppressed the production of pro-inflammatory cytokines (including interleukin-6, tumor necrosis factor-α and interleukin-1β), rebalanced levels of short-chain fatty acids and bile acids, improved gut barrier integrity and increased intestinal T regulatory cells. Directed chemical manipulation provides an additional tool for deciphering the chemical biology of the gut microbiome and might advance microbiome-targeted therapeutics.

2019-12-31 | GSE104913 | GEO

Directed Remodeling of the Mouse Gut Microbiome Inhibits the Development of Atherosclerosis [mouse tissue]

2019-12-31 | GSE104914 | GEO

Directed remodeling of the mouse gut microbiome inhibits the development of atherosclerosis.

| S-EPMC7641989 | biostudies-literature

Directed Remodeling of the Mouse Gut Microbiome Inhibits the Development of Atherosclerosis

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-12-31 | GSE104915 | GEO

A Novel Hidden Protein p-414aa Encoded by circSETD2(14,15) Inhibits Vascular Remodeling

Project description:The phenotypic switching of vascular smooth muscle cells (VSMCs) leads to neointimal hyperplasia, which is the underlying cause of vascular remodeling diseases such as atherosclerosis and hypertension. Novel hidden proteins encoded by circular RNAs (circRNAs) play crucial roles in disease progression. Our study identified a new protein derived from a circRNA in VSMCs and demonstrated its potential role in regulating vascular remodeling. We discovered a novel hidden protein, p-414aa, encoded by circSETD2(14,15), which can inhibit vascular remodeling. Both circSETD2(14,15) and p-414aa may serve as potential therapeutic targets for vascular remodeling diseases. In this study, we demonstrated that the new protein p-414aa encoded by circSETD2(14,15) inhibits VSMC proliferation and neointimal hyperplasia through the HuR/C-FOS axis. In summary, our data provide a molecular framework for the phenotypic switching of vascular smooth muscle cells.

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microbiome remodeling

Project description:Chemotherapeutic remodeling of the gut microbiome

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CCL17-expressing dendritic cells are crucial for the development of atherosclerosis

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

Ligustilide targets SMAD3, obstructing vascular fibrosis process in preventing atherosclerosis

Project description:Atherosclerosis is a persistent inflammatory state accompanied by lipid overload. Vascular fibrosis is one of the primary causes of atherosclerosis development. Although ligustilide (Lig) was shown to exert obvious antiatherogenic effects in previous studies, its precise mechanism has not been comprehensively discussed. In this paper, pharmacologic studies were performed to explore the pharmacodynamic effects of Lig on protecting aorta vascular wall structures and modulating serum inflammatory factors in ApoE-/- mice. Chemical proteomics based on a Lig-derived photoaffinity labelling (Lig-PAL) probe were applied to identify potential therapeutic targets. Mothers against decapentaplegic homologue 3 (SMAD3), which is closely related to the development of vascular fibrosis and atherosclerosis, was identified as a potential target of Lig. Lig suppressed the phosphorylation and nuclear translocation of SMAD3 by blocking the interaction between SMAD3 and transforming growth factor-β (TGF-β) receptor 1, thereby inhibiting the collagen synthesis process, preventing vascular fibrosis and improving atherosclerosis. The quantitative proteomics results from Lig-treated atherosclerotic ApoE-/- mice also indicated that Lig inhibits the expression of collagens I and III, interferes with collagen fibril organization processes and protects the aorta from vascular fibrosis. Hence, developing a novel SMAD3 inhibitor may present another therapeutic option for preventing atherosclerosis.

2020-01-21 | PXD017125 | Pride

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