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RNA-seq of mouse brain tissue to investigate the integrity of the blood brain barrier to trimethylamine N-oxide

ABSTRACT: RNA-seq of mouse brain tissue to investigate the integrity of the blood brain barrier to trimethylamine N-oxide

PROVIDER: PRJEB41818 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR4970152_1.fastq.gz	Fastqsanger.gz
	ERR4970152_2.fastq.gz	Fastqsanger.gz
	ERR4970153_1.fastq.gz	Fastqsanger.gz
	ERR4970153_2.fastq.gz	Fastqsanger.gz
	ERR4970154_1.fastq.gz	Fastqsanger.gz

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RNA-seq of mouse brain tissue to investigate the integrity of the blood brain barrier to trimethylamine N-oxide

Project description:In vivo work done to determine how trimethylamine N-oxide (TMAO) affects integrity of the blood-brain barrier. Wild-type male C57Bl/6 mice were injected with saline or TMAO (1.8 mg/kg in saline), and killed 2 h after injection. Mice were transcardially perfused with 0.9% saline at 4 °C to remove circulating blood, and brains were removed and collected into RNAlater. Whole brain total RNA was extracted using a PureLink RNA Mini Kit. RNA samples (n=3 TMAO, n=3 control) were sent to Macrogen Inc. (Republic of Korea) where they were subject to quality checks (RIN analysis), library prep and sequencing [TruSeq Stranded mRNA LT Sample Prep Kit; paired-end (2x 100 nt) sequencing; Illumina HiSeq 4000].

2020-12-19 | E-MTAB-9869 | biostudies-arrayexpress

Effects of gut-derived trimethylamines on an in vitro model of the blood–brain barrier

Project description:The experiment was designed to look at the effect (on gene expression) of exposing human cerebromicrovascular endothelial cell line hCMEC/D3 to trimethylamine (0.4 micromolar) or trimethylamine N-oxide (40 micromolar) for 24 h, to determine if circulating metabolites have the potential to affect integrity of the blood-brain barrier.

2019-10-31 | E-MTAB-6662 | biostudies-arrayexpress

Gut Microbiota-Derived Trimethylamine-N-Oxide Protects Pulmonary Vascular Barrier Integrity via VAV3-Mediated Cytoskeletal Remodeling in Acute Lung Injury

Project description:Acute respiratory distress syndrome (ARDS) and acute lung injury (ALI) are characterized by increased pulmonary capillary permeability, but lack effective pharmacotherapies. Emerging evidence implicates gut-lung axis dysregulation contributes to ARDS pathogenesis through microbiome-host interactions, but the effects of the microbiota-derived metabolite, trimethylamine-N-oxide (TMAO) remains unclear. Here, we demonstrate that plasma TMAO levels are significantly elevated in ARDS patients compared to healthy controls, correlating positively with hypersensitive C-reactive protein (hs-CRP). In a murine lipopolysaccharide (LPS)-induced ALI model, TMAO administration reduced lung vascular leakage and neutrophil infiltration, whereas inhibition of gut-microbiome-derived TMAO synthesis worsened injury. Mechanistically, TMAO enhances endothelial barrier integrity by upregulating VAV3, which drives Rac1-dependent cortical actin reorganization. Knockdown of VAV3 abolished TMAO-mediated endothelial barrier protection, confirming its necessity. Our study identifies TMAO as an adaptive mediator involved in gut-lung axis, that mitigates pulmonary vascular hyperpermeability via VAV3-Rac1-cytoskeletal signaling, highlighting its therapeutic potential for ALI/ARDS.

2025-09-23 | GSE308474 | GEO

Gut microbial metabolite trimethylamine N-oxide aggravates pulmonary hypertension

Project description:Trimethylamine N-oxide (TMAO), a metabolite derived from intestine microbial flora, enhances vascular inflammation in a variety of cardiovascular disease, and the bacterial communities associated with trimethylamine N-oxide (TMAO) metabolism is higher in pulmonary hypertension (PH) patients. The effects of TMAO on PH, however, has not been elucidated. In the present study, we found that circulating TMAO is elevated in intermediate to high-risk PH patients when compared to healthy control or low-risk PH patients. In monocrotaline-induced rat PH models, circulating TMAO is elevated; and reduction of TMAO using 3,3-dimethyl-1-butanol (DMB) significantly decreased right ventricle systolic pressure, pulmonary vascular muscularization in both monocrotaline-induced rat PH and hypoxia induced mice PH models. RNA sequencing of rat lungs on DMB revealed significant suppression of pathways involved in cytokine-cytokine receptor interaction, and cytokine and chemokine signaling. Protein-protein interaction analysis of the differentially expressed transcripts regulated by DMB showed 5 hub genes with a strong connectivity of proinflammatory cytokines and chemokines including Kng1, Cxcl1, Cxcl2, CxcL6 and Il6. In vivo, TMAO significantly increased the expression of Kng1, Cxcl1, Cxcl2, CxcL6 and Il6 in bone marrow derived macrophage. And TMAO-treated conditioned medium from macrophage increased the proliferation and migration of pulmonary artery smooth muscle cells; but TMAO treatment did not change the proliferation or migration of pulmonary artery smooth muscle cells. In conclusion, our study demonstrates that TMAO is increased in severe PH, and the reduction of TMAO using DMB reduces pulmonary vascular muscularization and alleviates PH via suppressing the macrophage production of chemokines and cytokines.

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Time-dependent specific molecular signatures of inflammation and remodelling are associated with Trimethylamine-N-oxide (TMAO)-induced endothelial cell dysfunction

Project description:Cardiovascular diseases (CVDs) are leading causes of death worldwide. Endothelial dysfunction is a critical initiating factor contributing to CVDs, which progression involves the gut microbiome-derived metabolite Trimethylamine N-oxide (TMAO). Here, we aim to clarify the time-dependent pathways by which TMAO mediates endothelial dysfunction.

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Gut microbial metabolite trimethylamine N-oxide aggravates pulmonary hypertension

Project description:Gut microbial metabolite trimethylamine N-oxide aggravates pulmonary hypertension

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Trimethylamine-N-oxide affects cell type-specific pathways and networks in mouse aorta to promote atherosclerotic plaque vulnerability

Project description:We performed single cell RNA-sequencing (scRNAseq) identify which aortic cell types, differentially expressed genes, and biological pathways are affected by trimethylamine-N-oxide (TMAO). We also modeled cell-cell communications and intracellular gene regulatory networks to identify gene networks perturbed by TMAO feeding. The objective of this study was to characterize the cell type-dependent and independent effects of TMAO on key vascular cell types involved in atherosclerosis progression in vivo.

2025-11-13 | GSE290376 | GEO

Trimethylamine N-oxide impairs β-cell function and glucose tolerance

Project description:Trimethylamine N-oxide impairs β-cell function and glucose tolerance

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Gut Microbiota-Derived Trimethylamine-N-Oxide Protects Pulmonary Vascular Barrier Integrity via VAV3-Mediated Cytoskeletal Remodeling in Acute Lung Injury

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Next Generation Sequencing of TMAO (Trimethylamine N-oxide)-treated Cardiac Transcriptomes

Project description:Next Generation Sequencing of TMAO (Trimethylamine N-oxide)-treated Cardiac Transcriptomes

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