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To investigate the effect of TMAO intervention on fatty liver cells in vitro and potential genetic changes

ABSTRACT: To construct the optimal fatty liver cell model in vitro and use TMAO intervention to observe its effect on fatty liver cells and identify potential key genes for change by transcriptomics.

ORGANISM(S): Homo sapiens

PROVIDER: GSE231368 | GEO | 2023/12/23

REPOSITORIES: GEO

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Gene expression levels after TMAO treatment

Project description:TMAO is gut microbiota dependent metabolite catalyzed by monooxygenase FMO3 from TMA. TMAO is positively assocaited with different metabolic diseases such as diabetes, chronic kidney disease, and atherosclerosis. We used microarray to analyze the genes regulated by TMAO treatment in primary rat hepatocytes to further understand the mechanistic view of TMAO action.

2019-08-22 | GSE135856 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of Hepa1-6 cells treated with 50 μM TMAO and 50ng/ml TNF-α Transcriptomes

Project description:Liver cancer has a high mortality rate. Chronic inflammation is one of the leading causes of hepatocellular carcinoma. Recent studies suggested high levels of trimethylamine N-oxide (TMAO) may correlate with increased risk of inflammatory-induced liver cancer. However, the mechanisms by which TMAO promotes liver cancer remain elusive. Here, we established a model of inflammatory-induced liver cancer by treating Hepa1-6 cells with TNF-α. TMAO synergistically increased the proliferation, migration and invasion of Hepa1-6 cells in the presence of TNF-α. We conducted bulk RNA-Seq of the TMAO-treated cell model of inflammatory Hepatocellular carcinoma (HCC)

2022-01-18 | GSE193557 | GEO

Transcription profiling of liver from wistar and kyoto rats exposed to orotic acid to investigate fatty liver disease

Project description:Although fatty liver disease is caused by a number of toxicological insults and the metabolic syndrome, the exact mechanisms by which many of these pathophysiological stimulii induce fatty liver are unknown. The rapid and profound steatosis caused by orotic acid, resulting from an impairment in the production of ApoB, has been investigated in the Wistar strain rat using a combined transcriptomic and metabonomic/metabolomic approach. Analysis of liver tissue from rats exposed to orotic acid for 1, 3, and 14 days was performed by DNA microarrays and high resolution 1H NMR spectroscopy based metabonomics of both tissue extracts and intact tissue (n = 3). Data were analyzed using a combination of ANOVA and principal components analysis, used as a data reduction tool to visualize the most perturbed transcripts and metabolites. Orotic acid produced a profound 8-fold increase in total lipids, and in particular increases in resonances associated with polyunsaturated fats (CHCH and CH2CHCH groups). This was accompanied by increases in the concentrations of trimethylamine-oxide (TMAO), betaine, choline, and phosphocholine, as well as a relative decrease in glucose and glycogen. At the transcriptional level, perturbations were detected in both oxidative stress and osmoregulation/pH homeostasis. However, this contrasts with a previous transcriptomic/metabolic study of fatty liver disease in a combined data set of Wistar (out-bred) and Kyoto (in-bred) strains of rats, with only 4 transcripts being found to be in common between the two analyses. This emphasizes the need to understand how strain background interacts with a given toxic lesion or genetic modification. Keywords: metabolomics . metabolic profiling . pattern recognition . nonalcoholic steatohepatisis

2009-03-11 | E-BIID-1 | biostudies-arrayexpress

The TMAO Generating Enzyme Flavin Monooxygenase 3 is a Central Regulator of Cholesterol Balance

Project description:Circulating levels of the gut microbe-derived metabolite trimethylamine-N-oxide(TMAO) have recently been linked to cardiovascular disease (CVD) risk. Here we performed transcriptional profiling in mouse models of altered reverse cholesterol transport (RCT), and serendipitously identified the TMAO-generating enzyme flavin monooxygenase 3 (FMO3) as a powerful modifier of cholesterol metabolism and RCT. Knockdown of FMO3 in cholesterol-fed mice alters biliary lipid secretion, blunts intestinal cholesterol absorption, and limits the production of hepatic oxysterols and cholesteryl esters. Furthermore, FMO3 knockdown stimulates basal and liver X receptor (LXR)-stimulated macrophage RCT, thereby improving cholesterol balance. Conversely, FMO3 knockdown exacerbates hepatic ER stress and inflammation in part by decreasing hepatic oxysterol levels and subsequent LXR activation. FMO3 is thus identified as a central integrator of hepatic cholesterol and triacylglycerol metabolism, inflammation, and ER stress. These studies suggest that the gut microbiota-driven TMA/FMO3/TMAO pathway is a key regulator of lipid metabolism and inflammation. To identify potential regulators of macrophage reverse cholesterol transport (RCT), liver was isolated from two independent mouse models where the non-biliary RCT pathway known as transintestinal cholesterol excretion (TICE) was either chronically (NPC1L1-liver-transgenic mice) or acutely (ACAT2 antisense oligonucleotide treatment) stimulated. Total RNA was isolated and gene expression levels were profiled on the Affymetrix GeneAtlas MG-430 PM Array Strip (Affymetrix; Santa Clara, CA, USA)

2014-12-19 | E-GEOD-64326 | biostudies-arrayexpress

TMAO promoted TREM-1 expression through NLRP3 inflammasome

Project description:To investigate the impact of TMAO on Myeloid cells. An RNA-seq analysis of myeloid cells was performed with and without TMAO treatment.

2023-12-18 | GSE250419 | GEO

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

Project description:To investigate the mechanism how TMAO deteriorates cardiac dysfunction in murine left ventricular pressure overload model, we performed RNA-seq analysis with cardiac tissue from TMAO-treated mice.

2020-04-01 | GSE129756 | GEO

fatty liver

Project description:fatty liver tissue sequencing

| PRJNA515852 | ENA

Transcriptional profiling of trimethylamine N-oxide (TMAO) stimulated human aortic endothelial cells (HAECs)

Project description:Purpose: The goals of this study were to identify preferential gene expression signatures that are unique to HAECs stimulated with the uremic toxin, TMAO, to accelerate vascular inflammation associated with chronic kidney diseases. Methods and results: HAECs were treated with TMAO (600 µM) for 18 hours, and RNAs were collected to generate mRNA transcription profiles. Transcriptional profiling revealed a unique TMAO stimulated HAECs relative to a non-stimulated control HAECs. Conclusion: Our study represents the first detailed analysis of TMAO treated HAECs transcriptome.

2023-01-03 | GSE216833 | GEO

TMAO treated human vascular smooth muscle cells

Project description:We utilized human aortic vascular smooth muscle cells (HAVSMCs) treated with saline or trimethylamine N-oxide (TMAO) for 5 hours

2023-01-02 | GSE200143 | GEO

The TMAO Generating Enzyme Flavin Monooxygenase 3 is a Central Regulator of Cholesterol Balance

2014-12-19 | GSE64326 | GEO

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