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Effect of 4-octyl itaconate on gene expression of dendritic cells

ABSTRACT: Effect of 4-octyl itaconate on gene expression of dendritic cells

PROVIDER: PRJNA1117028 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29195510_1.fastq.gz	Fastqsanger.gz
	SRR29195510_2.fastq.gz	Fastqsanger.gz
	SRR29195511_1.fastq.gz	Fastqsanger.gz
	SRR29195511_2.fastq.gz	Fastqsanger.gz
	SRR29195512_1.fastq.gz	Fastqsanger.gz

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Effect of 4-octyl itaconate on gene expression of dendritic cells

Project description:Here, we report that macrophage-derived itaconate exerts a significant suppressive effect on dendritic cell (DC) function. To delve deeper into the impact of itaconate on DCs, we treated bone marrow-derived dendritic cells with 4-OI, a derivative of itaconate, and conducted RNA-seq analysis. Gene-set enrichment analysis (GSEA) of 4-OI-treated DCs showed a general downregulation of innate immunity and immune-response pathways.

2024-06-30 | GSE268402 | GEO

RNA-seq Transcriptomic Analysis of 4-octyl itaconate Repressing Myogenic Differentiation

Project description:The 4-octyl itaconate O1_is a type of cell-permeable itaconate derivative. Studies have shown that with an anti-fibrotic effect in systemic sclerosis, the OI also affects osteoclast differentiation. The aim of this study was to explore the molecular mechanisms underlying the effects of OI on myoblast differentiation by RNA-seq analysis.

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Single-cell RNA sequencing analysis of the effect of 4-octyl itaconate administration on gene expression in immune cells isolated from traumatic brain injury mice brain

Project description:4-octyl itaconate regulates immune response of brain immune cells following traumatic brain injury.

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Expression data from hiPSC derived WT and ISG15 KO endothelial cells stimulated with interferon-a and treated with itaconic acid, dimethyl itaconate, 4-octyl itaconate and ruxolitinib

Project description:Analysis of gene expression in WT and ISG15 KO endothelial cells, stimulated with IFNa and treated with Itaconic acid (IA), Dimethyl itaconate (DI), 4-octyl itaconate (4OI) and ruxolitinib (RUX) to investigate the effects of treatments on transcriptional response in the cells.

2022-06-07 | GSE168747 | GEO

10x single-cell RNAseq profiling of hiPSC derived WT and ISG15 KO macrophages stimulated with interferon-a and treated with itaconic acid, 4-octyl itaconate and ruxolitinib

Project description:WT and ISG15 KO macrophages were stimulated with interferon-a and treated with itaconic acid and 4-octyl itaconate as they are known for anti-inflammatory effects. In this experiment, we further explored how itaconic acid and 4-octyl itaconate can play its role keeping ruxolitinib as a positive control in order to inhibit JAK/STAT pathway

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Endogenous itaconate is not required for particulate matter-induced NRF2 expression or inflammatory response

Project description:RNA-sequencing demonstrated Acod1 (Aconitate decarboxylase 1) as one of the top genes induced by air polution particulate matter (PM) in macrophages. We therefore sought to determine the effect of both exogenous itaconate (4-octyl itaconate) and endogenous itaconate on PM-induced inflammation in macrophages through RNA sequencing.

2020-04-07 | GSE143881 | GEO

Expression data from PBMCs infected with influenza A virus and treated with/without Itaconate

Project description:Analysis of gene expression in human PBMCs infected with influenza A virus or Mock and treated with Itaconic acid, Dimethyl itaconate or 4-Octyl itaconate to investigate the effects itaconate have on transcriptional response in human PBMCs. We particularly looked at anti-inflammatory effects of itaconate in inflammation followed by Influenza A virus infection.

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RNA-seq Transcriptomic Analysis of 4-octyl itaconate Repressing Myogenic Differentiation

Project description:RNA-seq Transcriptomic Analysis of 4-octyl itaconate Repressing Myogenic Differentiation

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4-octyl itaconate inhibits aerobic glycolysis by targeting GAPDH to exert anti-inflammatory effects

Project description:Activated macrophages switch from oxidative phosphorylation to aerobic glycolysis, similar to the Warburg effect, presenting a potential therapeutic target in inflammatory disease. The endogenous metabolite itaconate has recently been reported to regulate macrophage function, but its precise mechanism is not fully understood. Here, we showed that 4-octyl itaconate (OI, a cell-permeable itaconate derivative) directly alkylated cysteine residue 22 on the glycolytic enzyme GAPDH and decreased its enzyme activity. Glycolytic flux analysis by U13C‐glucose tracing also provided evidence that OI generated a blockade of glycolytic flux at GAPDH. OI thereby downregulates aerobic glycolysis in activated macrophages, which is required for its anti-inflammatory effects. The anti-inflammatory effects of OI were replicated by heptelidic acid, 2-DG and reversed by increasing wild-type but not C22A mutant GAPDH expression. OI protected against lipopolysaccharide-induced lethality in vivo and significantly inhibited cytokine release. These findings showed that itaconate is a critical immunometabolite that exerts anti-inflammatory effects by targeting GAPDH to decrease aerobic glycolysis in macrophages.

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2024-06-28 | GSE221734 | GEO

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