Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ACCESS DATA

Json Xml

Dataset's files

Source:

			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

Items per page:

1 - 5 of 21

Similar Datasets

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

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

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

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

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

Fecal bbu genes predict L-carnitine-mediated TMAO production

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

| PRJEB66719 | ENA

Intrinsic TGF-b Signaling Attenuates Proximal Tubule Mitochondrial Injury and Inflammation in Chronic Kidney Disease

Project description:Intrinsic TGF-b Signaling Attenuates Proximal Tubule Mitochondrial Injury and Inflammation in Chronic Kidney Disease

| PRJNA936155 | ENA

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 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

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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data