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Trimethylamine oxide is a new plant signaling molecule that mediates abiotic stress tolerance

ABSTRACT: We report the identification of RCI5, an Arabidopsis cold inducible gene encoding a FMO. RCI5 seems to participate in the biosynthesis of TMAO, a new plant methabolite. We also demonstrate that TMAO positevely controls Arabidopsis tolerance to low temperature, high salt in the soil and drough stress, by promoting a wide transcriptomic reprograming of stress-relate genes. Finally, we found that diferent crops also contain TMAO in their tissues, and that exogenous applications of TMAO also increases tomato tolerance to abiotic stress.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE144502 | GEO | 2021/05/26

REPOSITORIES: GEO

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

Project description:β-Cell dysfunction, manifested as impaired glucose-stimulated insulin secretion (GSIS), and β-cell loss, which presents as dedifferentiation, inhibited transcriptional identity and death, are the hallmarks of type 2 diabetes. Trimethylamine N-oxide (TMAO), a gut microbiota metabolite, has been shown to play a role in cardiovascular disease. Here, we found that plasma TMAO levels are elevated in both diabetic mice and human subjects and that TMAO at a similar concentration to that found in diabetes could directly decrease β-cell GSIS in both MIN6 cells and primary islets from mice or humans. Elevation of TMAO levels through choline diet feeding impairs GSIS, the β-cell proportion, and glucose tolerance. TMAO inhibits calcium transients through NLRP3 inflammasome-related inflammatory cytokines and induced Serca2 loss, and a Serca2 agonist reversed the effect of TMAO on β-cell function in vitro and in vivo. Additionally, long-term TMAO exposure promotes β-cell ER stress, dedifferentiation, and apoptosis and inhibits β-cell transcriptional identity. Inhibition of TMAO production through either genetic knockdown or antisense oligomers of Fmo3, the TMAO-producing enzyme, improves β-cell GSIS, the β-cell proportion, and glucose tolerance in both db/db and choline diet-fed mice. These observations elucidate a novel role for TMAO in β-cell dysfunction and maintenance, and inhibition of TMAO could be a new approach for the treatment of type 2 diabetes.

2024-02-23 | GSE243083 | 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.

2022-06-07 | GSE190203 | 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

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

Transcriptional changes in Escherichia coli during a shift from fermentation to Trimethylamine-N-oxide (TMAO) respiration

Project description:Gene-expression measurements were made over a 24 h time course as fermentative steady state E. coli cells were subjected to a shift to TMAO respiration.

2014-12-13 | E-MTAB-2784 | biostudies-arrayexpress

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

The effect of trimethylamine N-oxide on the metabolism of visceral white adipose tissue in spontaneously hypertensive rat

Project description:Male SHRs and normotensive Wistar-Kyoto(WKY) rats were purchased from Vital River (Vital River Laboratory Animal Technology Co., Ltd, Beijing, China). Briefly, eightteen SHRs aged seven to eight weeks old were randomly assigned to one of three groups: water group (drinking tap water), water containing 333 mg/L or 1g/L TMAO group (TMAO, product number: T1362, Tokyo Chemical Industry, Japan). Six WKY rats of the same age were used as normotensive controls. In this study, WKY rats (n=6), SHR (n=6), and SHR treated with 1g/L TMAO (n=6) were uesd for experiments.

2022-08-17 | GSE188336 | GEO

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.

2023-11-23 | GSE235204 | GEO

Trimethylamine oxide is a new plant signaling molecule that mediates abiotic stress tolerance

Project description:Trimethylamine oxide is a new plant signaling molecule that mediates abiotic stress tolerance

| PRJNA603806 | ENA

Intestinal microbiota composition modulates choline bioavailability from diet and accumulation of the pro-atherogenic metabolite trimethylamine-N-oxide

Project description:Choline is a water-soluble nutrient essential for human life. Gut microbial metabolism of choline results in the production of trimethylamine (TMA), which upon absorption by the host is converted in the liver to trimethylamine N-oxide (TMAO). Recent studies revealed that TMAO exacerbates atherosclerosis in mice, and positively correlates with the severity of this disease in human. However, which microbes contribute to TMA production in the human gut; the extent to which host factors, e.g., genotype and diet, affect TMA production and colonization of these microbes; as well as the effects TMA-producing microbes have on bioavailability of dietary choline remain largely unknown. We screened a collection of 78 sequenced human intestinal isolates encompassing the major phyla found in the human gut and identified eight strains capable of producing TMA from choline in vitro. Gnotobiotic mouse studies showed that TMAO accumulates in the serum of animals colonized with TMA-producing species, but not in the serum of animals colonized with intestinal isolates that do not generate TMA from choline in vitro. Remarkably, low levels of colonization of TMA-producing bacteria significantly reduced choline levels available to the host. This effect was more pronounced as the abundance of TMA-producing bacteria increased. Our findings provide a framework for designing strategies aimed at changing the representation or activity of TMA-producing bacteria in the human gut and suggest the TMA producing status of the gut microbiota should be considered when making recommendations about choline intake requirements for humans.

2015-04-02 | GSE63461 | GEO

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