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Mus musculus

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

PROVIDER: PRJNA371732 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5237160.fastq.gz	Fastqsanger.gz
	SRR5237161.fastq.gz	Fastqsanger.gz
	SRR5237159.fastq.gz	Fastqsanger.gz
	SRR6177790.fastq.gz	Fastqsanger.gz
	SRR6177791.fastq.gz	Fastqsanger.gz

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

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

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

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

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KDM4B epigenetically protects against obesity and metabolic dysfunction [gene expression]

Project description:KDM4B (lysine demethylase 4B) in adipose tissues plays a critical role in energy balance, oxidation, lipolysis and thermogenesis. Loss of KDM4B in mice resulted in obesity associated with reduced energy expenditure and impaired adaptive thermogenesis. Mechanistically, we determined that KDM4B directly controls the expression of multiple metabolic genes.

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Cancer-cell-secreted miR-204-5p induces leptin signaling pathway in white adipose tissue to promote cancer-associated cachexia

Project description:Cachexia is a wasting disorder of adipose tissues that leads to profound weight loss and frailty. One key characteristic of cachexia is elevated resting energy expenditure, which has been linked to increased fat lipolysis and thermogenesis.

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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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