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IL-10 signaling remodels adipose chromatin architecture to limit thermogenesis and energy expenditure

ABSTRACT: IL-10 signaling remodels adipose chromatin architecture to limit thermogenesis and energy expenditure

PROVIDER: PRJNA371736 | ENA |

REPOSITORIES: ENA

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IL-10 signaling remodels adipose chromatin architecture to limit thermogenesis and energy expenditure [ChIP-Seq]

Project description:IL-10 signaling remodels adipose chromatin architecture to limit thermogenesis and energy expenditure [ChIP-Seq]

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IL-10 signaling remodels adipose chromatin architecture to limit thermogenesis and energy expenditure [RNA-Seq]

Project description:Signaling pathways that promote adipose tissue thermogenesis are well characterized, but the physiologic limiters of energy expenditure are largely unknown. Here we show that ablation of the anti-inflammatory cytokine IL-10 improves insulin sensitivity, protects against diet-induced obesity, and elicits the browning of white adipose tissue. Mechanistic studies define bone marrow cells as the source of the IL-10 signal and mature adipocytes as the target cell type mediating these effects. IL-10 receptor alpha is highly enriched in mature adipocytes and is induced in response to cold, obesity and aging. ATAC-seq and RNA-seq reveal that IL-10 represses the transcription of thermogenic genes in adipocytes by altering chromatin accessibility and inhibiting ATF and PGC-1alpha recruitment to key enhancer regions. These findings identify the IL-10 axis as a critical and potentially targetable regulator of thermogenesis, and expand our understanding of the links between inflammatory signaling and adipose tissue function in the setting of obesity.

2018-01-28 | GSE94653 | GEO

IL-10 signaling remodels adipose chromatin architecture to limit thermogenesis and energy expenditure [ATAC-Seq]

2018-01-28 | GSE94651 | GEO

IL-10 signaling remodels adipose chromatin architecture to limit thermogenesis and energy expenditure [ChIP-Seq]

2018-02-27 | GSE111208 | GEO

IL-10 Signaling Remodels Adipose Chromatin Architecture to Limit Thermogenesis and Energy Expenditure.

Project description: Not available

| S-EPMC5766418 | biostudies-literature

IL-10 signaling remodels adipose chromatin architecture to limit thermogenesis and energy expenditure

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-01-28 | GSE94654 | GEO

Ablation of TET proteins in adipocytes protects against adiposity and metabolic dysfunction by potentiating energy expenditure

Project description:Ten-eleven translocation (TET) proteins oxidize 5-methylcytosine in DNA to 5- hydroxymethylcytosine and further oxidized derivatives. Here we show that TET proteins are key epigenetic suppressors of adipocyte thermogenesis and energy expenditure in both white and brown adipose tissues in vivo. Tet expression in adipocytes decreases upon cold or adrenergic stimulation but increases following high-fat diet (HFD) consumption. Mice with triple deletion of all three Tet genes in adipocytes have higher energy expenditure due to enhanced fat browning and thermogenesis. They also show significantly enhanced lipolysis because of elevated expression of Adrb3 and key lipases including Atgl and Hsl. Consequently, the knockout mice display improved cold tolerance and are substantially resistant to obesity, inflammation, and associated metabolic complications including insulin resistance. Mechanistically, TET deficiency substantially prevents the HFD-induced transcriptional alterations in adipose tissues. TET proteins recruit histone deacetylases (HDACs) to the key thermogenic gene loci including Adrb3, Ppargc1a, and Ucp1, leading to transcriptional repression through histone deacetylation. Thus, the TET-HDAC axis may be therapeutically targeted to treat obesity and related metabolic diseases.

2021-11-01 | GSE178762 | GEO

Mus musculus

Project description:IL-10 signaling remodels adipose chromatin architecture to limit thermogenesis and energy expenditure [ATAC-Seq]

| PRJNA371732 | ENA

Mus musculus

Project description:IL-10 signaling remodels adipose chromatin architecture to limit thermogenesis and energy expenditure [RNA-Seq]

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The Innate Immune Factor IRF3 Reduces Adipose Thermogenesis via ISG15-mediated Reprogramming of Cellular Metabolism

Project description:Purpose: Interferon regulatory factor 3 (IRF3) is activated by pro-inflammatory cytokines, but its role in regulating adaptive thermogenesis and energy expenditure remains unclear. Here, we report that IRF3 as a negative transcription regulator of adaptive thermogenesis. Adipocyte-specific IRF3 knockout (FI3KO) attenuates HFD-induced obesity by increasing energy expenditure; further studies show that IRF3 suppresses adaptive thermogenesis through ISG15-mediated inhibition of glycolysis in adipocytes. Conversely, overexpression of IRF3 in adipocytes causes reduced thermogenesis gene expression, energy expenditure, and more persistent to HFD-induced obesity. Moreover, Isg15-/- increases adipose thermogenesis and protects mice from HFD-induced obesity and glucose intolerance. Taken together, these data indicate that IRF3 as a transcriptional regulator connecting between inflammatory signaling pathway and energy homeostasis Methods: primary adipocyte mRNA profiles of 8-week-old wild-type (WT) and FI3OE mice were generated by deep sequencing. The sequence reads that passed quality filters were analyzed at the transcript isoform level. qRT–PCR validation was performed using RT-PCR. Conclusions: Our study represents the first detailed analysis of adipocyte transcriptomes from WT and FI3OE iWAT, with biologic replicates, generated by RNA-seq technology. The optimized data analysis workflows reported here should provide a framework for comparative investigations of expression profiles. Our results show that Irf3 adipocyte-speficic overrxpression markedly increases the expression of Isg15 and Herc6, which play important role in regulation of glycolysis.

2020-07-24 | GSE155019 | GEO

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