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

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

PROVIDER: PRJNA964593 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24364700_1.fastq.gz	Fastqsanger.gz
	SRR24364700_2.fastq.gz	Fastqsanger.gz
	SRR24364701_1.fastq.gz	Fastqsanger.gz
	SRR24364701_2.fastq.gz	Fastqsanger.gz
	SRR24364696_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

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

Project description: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.

2023-12-23 | GSE231368 | 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

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

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

Counteracting Osteoclastic Resorption and Development of Osteoporosis via Rebalancing Gut Microbiota and thus Metabolite TMAO by Traditional Decoction Medicine

Project description:Osteoporosis represents a significant health challenge, particularly in postmenopausal women. While traditional medicine offers potential solutions, the mechanisms underlying their efficacy remain elusive. This study demonstrates the bone-protective properties of Guilu Erxian gel decoction (GEX), a traditional medicine prepared from tortoise plastron, antler, and herbs, by elucidating its impact on gut microbiota and associated metabolites. Using an ovariectomized mouse model of postmenopausal osteoporosis, we demonstrate that GEX consumption significantly reduces key osteoporotic markers, including low bone mineral density, compromised trabecular microstructure, and reduced biomechanical strength. GEX intake profoundly reshapes the gut microbiome, enriching beneficial bacteria crucial for fatty acid metabolism and mineral absorption. Gut microbiota transplantation from GEX-fed mice to ovariectomized recipients reversed probiotic bacterial abundance, particularly Bifidobacterium and Akkermansia. This intervention effectively alleviated ovariectomy-induced colon inflammation, trimethylamine N-oxide (TMAO) overproduction, and osteoporosis progression. Excessive TMAO promotes osteoclastogenic differentiation in macrophages in vitro. Using μCT imaging, biomechanical testing, histological staining, and 16S rRNA sequencing, we provide compelling evidence for the complex therapeutic effects of GEX, including mitigation of osteoclast overburden, reduction of marrow adiposis, suppression of RANKL overproduction, and preservation of colon goblet cell mucin. This study demonstrates the interplay between gut microbiota, its metabolite TMAO, and bone health, offering new insights into the mechanism of action of GEX. Our findings not only validate the bone-protective potential of this traditional medicine but also open new avenues for developing microbiome-based strategies to combat osteoporosis.

2025-08-16 | GSE294739 | GEO

Adipocyte FMO3-derived TMAO induces WAT dysfunction and metabolic disorders by promoting inflammasome activation in ageing

Project description:Circulating trimethylamine N-oxide (TMAO) participates in the pathogenesis of cardio-metabolic diseases, with hepatic flavin-containing monooxygenase 3 (FMO3) originally regarded as the primary source of TMAO production. Here, we demonstrate that white adipose tissue (WAT) expressed FMO3 and its derived metabolic product TMAO causatively contribute to the systemic elevation of TMAO levels, WAT dysfunction, and metabolic diseases in ageing. We showed that FMO3 expression and TMAO levels are upregulated in WAT of naturally ageing animals and human subjects, as well as in a DNA damage-induced senescent adipocyte model, but not in the liver. This upregulation is due to p53 activation in mice and could be mitigated by calorie restriction in humans. Adipocyte-specific ablation of FMO3 attenuates TMAO accumulation in WAT and circulation, leading to enhanced glucose metabolism, energy homeostasis, and lipid regulation in aged and high-fat diet-induced obese mice. Transcriptomic and histological analysis link these metabolic improvements to reduced senescence, fibrosis, and inflammation in WAT as well as a decrease in adipose-resident macrophages. LiP-small molecule mapping (LiP-SMap) analysis identified numerous novel TMAO-interacting proteins implicated in inflammasome activation within white adipocytes and macrophages. Mechanistically, TMAO facilitates inflammasome activation by binding to the inflammasome adaptor protein apoptosis-associated speck-like protein containing A CARD (ASC), thereby inducing its expression, caspase-1 activation, and subsequent interleukin-1β (IL-1β) production. Our findings uncover a pivotal role for adipocyte FMO3 in modulating TMAO production and WAT dysfunction by promoting inflammasome activation in ageing via an autocrine and paracrine manner.

2025-08-23 | PXD066391 | Pride

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

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

TMAO promotes NLRP3 inflammasome activation of microglia aggravating neurological injury in stroke through FTO/IGF2BP2

Project description:Stroke is a kind of cerebrovascular disease with high mortality. TMAO has been shown to aggravate stroke outcomes, but its mechanism remains unclear. Mice were treated with TMAO in normal saline by oral gavage for 14 consecutive days. Then, mice were made into MCAO models. Neurological score, infarct volume, neuronal damage and markers associated with inflammation were assessed. Since microglia played a crucial role in stroke, microglia of MCAO mice were isolated for high-throughput sequencing to identify the most differentially expressed gene following TMAO treatment. Afterward, the downstream pathways of TMAO were investigated using primary microglia. Our results demonstrated that TMAO promoted the release of inflammatory cytokines in the brain of MCAO mice and promoted the activation of OGD/R microglial inflammasome, thereby exacerbating stroke outcomes. FTO/IGF2BP2 inhibited NLRP3 inflammasome activation in OGD/R microglia by downregulating the m6A level of NLRP3, TMAO can inhibit the expression of FTO and IGF2BP2, thus promoting the activation of NLRP3 inflammasome in OGD/R microglia. In conclusion, these results demonstrated that TMAO promotes NLRP3 inflammasome activation of microglia aggravating neurological injury in stroke through FTO/IGF2BP2.

2023-09-06 | GSE216349 | GEO

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