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Inhibition of microbiota-dependent TMAO production attenuates chronic kidney disease in mice

ABSTRACT: Inhibition of microbiota-dependent TMAO production attenuates chronic kidney disease in mice

PROVIDER: PRJNA685459 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13296261.fastq.gz	Fastqsanger.gz
	SRR13296262.fastq.gz	Fastqsanger.gz
	SRR13296263.fastq.gz	Fastqsanger.gz
	SRR13296264.fastq.gz	Fastqsanger.gz
	SRR13296265.fastq.gz	Fastqsanger.gz

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Inhibition of microbiota-dependent TMAO production attenuates chronic kidney disease in mice

Project description:Methods: RNA-seq analysis was performed on mouse kidney samples isolated from female apoEKO mice on 4 diets for 14 weeks: (1) Control diet, (2) control + iodomethylcholine (IMC), Control + IMC. IMC is a TMA-lyase inhibitor to prevent TMA production by gut

2021-01-19 | GSE163276 | GEO

Inhibition of microbiota-dependent TMAO production attenuates chronic kidney disease in mice.

Project description:Patients with chronic kidney disease (CKD) have elevated circulating levels of trimethylamine N-oxide (TMAO), a metabolite derived from gut microbes and associated with cardiovascular diseases. High circulating levels of TMAO and its dietary precursor, choline, predict increased risk for development of CKD in apparently healthy subjects, and studies in mice fed TMAO or choline suggest that TMAO can contribute to kidney impairment and renal fibrosis. Here we examined the interactions between TMAO, kidney disease, and cardiovascular disease in mouse models. We observed that while female hyperlipidemic apoE KO mice fed a 0.2% adenine diet for 14 weeks developed CKD with elevated plasma levels of TMAO, provision of a non-lethal inhibitor of gut microbial trimethylamine (TMA) production, iodomethylcholine (IMC), significantly reduced multiple markers of renal injury (plasma creatinine, cystatin C, FGF23, and TMAO), reduced histopathologic evidence of fibrosis, and markedly attenuated development of microalbuminuria. In addition, while the adenine-induced CKD model significantly increased heart weight, a surrogate marker for myocardial hypertrophy, this was largely prevented by IMC supplementation. Surprisingly, adenine feeding did not increase atherosclerosis and significantly decreased the expression of inflammatory genes in the aorta compared to the control groups, effects unrelated to TMAO levels. Our data demonstrate that inhibition of TMAO production attenuated CKD development and cardiac hypertrophy in mice, suggesting that TMAO reduction may be a novel strategy in treating CKD and its cardiovascular disease complications.

| S-EPMC7804188 | biostudies-literature

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

Fecal bbu genes predict L-carnitine-mediated TMAO production

Project description:Fecal bbu genes predict L-carnitine-mediated TMAO production

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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 Suppresses Megalin Expression and Albumin Uptake in Human Proximal Tubular Cells Via PI3K and ERK Signaling

Project description:Trimethylamine-N-oxide (TMAO) is a uremic toxin, which has been associated with chronic kidney disease (CKD). Renal tubular epithelial cells play a central role in the pathophysiology of CKD. Megalin is an albumin-binding surface receptor on tubular epithelial cells, which is indispensable for urine protein reabsorption. To date, no studies have investigated the effect of TMAO on megalin expression and the functional properties of human tubular epithelial cells. The aim of this study was first to identify the functional effect of TMAO on human renal proximal tubular cells and second, to unravel the effects of TMAO on megalin-cubilin receptor expression. We found through global gene expression analysis that TMAO was associated with kidney disease. The microarray analysis also showed that megalin expression was suppressed by TMAO, which was also validated at the gene and protein level. High glucose and TMAO was shown to downregulate megalin expression and albumin uptake similarly. We also found that TMAO suppressed megalin expression via PI3K and ERK signaling. Furthermore, we showed that candesartan, dapagliflozin and enalaprilat counter-acted the suppressive effect of TMAO on megalin expression. Our results may further help us un-ravel the role of TMAO in CKD development and to identify new therapeutic targets to counteract TMAOs effects.

2022-08-10 | GSE210692 | GEO

7-Hydroxycoumarin attenuates colistin-induced kidney injury in mice through the inhibition of HDAC1 and the activation of Nrf2 signaling

Project description:RNA sequencing of kidney tissues was performed to investigate the mechanism of 7-Hydroxycoumarin attenuates colistin-induced kidney injury in mice

2020-05-14 | GSE150518 | GEO

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

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

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

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