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TMAO promoted TREM-1 expression through NLRP3 inflammasome

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

ORGANISM(S): Mus musculus

PROVIDER: GSE250419 | GEO | 2023/12/18

REPOSITORIES: GEO

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TMAO promoted TREM-1 expression through NLRP3 inflammasome

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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.

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Gene expression levels after TMAO treatment

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

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

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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.

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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.

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

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The Ragulator complex regulates NLRP3 inflammasome activation through interaction with HDAC6

Project description:The activation of the NLRP3 inflammasome is spatiotemporally orchestrated by various organelles, but the precise roles of lysosomes are still unclear. Here we show the vital role of the Ragulator complex, a lysosomal protein, in NLRP3 inflammasome activation. Deficiency of Lamtor1, an essential component of the Ragulator complex, abrogated NLRP3 inflammasome activation in murine macrophage and human monocytic cells. Myeloid-specific Lamtor1-deficient mice showed remarkable attenuation of the severity of NLRP3-associated inflammatory diseases, including LPS-induced sepsis, alum-induced peritonitis, and monosodium urate (MSU)-induced arthritis. Mechanistically, Lamtor1 interacted with histone deacetylase 6 (HDAC6) during NLRP3 inflammasome activation, and this interaction augmented the interaction between the Ragulator complex and NLRP3. Lack of HDAC6 attenuated the interaction between Lamtor1 and NLRP3, resulting in insufficient NLRP3 inflammasome activation. Furthermore, DL-all-rac-α-tocopherol inhibited Lamtor1–HDAC6 interaction, resulting in diminished NLRP3 inflammasome activation. DL-all-rac-α-tocopherol alleviated acute gouty arthritis and MSU-induced peritonitis. Our results provide insight into the role of lysosomes in providing a platform for the activation of NLRP3 inflammasomes by the Ragulator complex.

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