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Stat1 activation, through systemic interferon signaling, and upregulation of innate immune system receptors drives inflammaging, that is ameliorated by dietary restriction intervention [ATAC-seq]

ABSTRACT: Stat1 activation, through systemic interferon signaling, and upregulation of innate immune system receptors drives inflammaging, that is ameliorated by dietary restriction intervention [ATAC-seq]

PROVIDER: PRJNA682754 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13202512.fastq.gz	Fastqsanger.gz
	SRR13202513.fastq.gz	Fastqsanger.gz
	SRR13202514.fastq.gz	Fastqsanger.gz
	SRR13202515.fastq.gz	Fastqsanger.gz
	SRR13202516.fastq.gz	Fastqsanger.gz

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Stat1 activation, through systemic interferon signaling, and upregulation of innate immune system receptors drives inflammaging, that is ameliorated by dietary restriction intervention [RNA-seq]

Project description:Aging is the result of an accumulation of molecular damages, driven by multiple factors like metabolic and oxidative stress, (epi)genetic alterations, and microbiome dysbiosis. In addition, aging is characterized by a chronic, low-grade inflammation known as inflammaging that represents a high significant risk factor for most, if not all, age-related diseases. Dietary restriction (DR) is the best-known non-invasive method to ameliorate the aging phenotype in many organisms. While it has been shown that DR reduces the inflammation in some tissues, the molecular mechanisms in old individuals are still largely unknown. Here we identify a multi-tissue gene network which regulates the inflammaging and that is ameliorated by DR. Using transcriptional profiling (RNA-seq), we found that aging upregulates the innate immune system receptor together with the activation of a systemic interferon (IFN) signaling through the Interferon Regulatory Factors (Irf), inflammatory cytokines and finally Stat1 transcription factor. Our results suggest that DR is able to ameliorate inflammaging by downregulating the expression and the activity of almost all the components of this gene network. In addition, chromatin accessibility genome-wide analysis showed that the binding site of Irf and Stat1 in the promoter of their target genes are more open in aging and become closer upon DR treatment indicating a transcriptional control of the inflammaging phenotype involving epigenetic modifications. Our results provide a comprehensive understanding of the molecular network regulating the inflammation in aging and DR and present novel anti-inflammaging therapeutic targets.

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Stat1 activation, through systemic interferon signaling, and upregulation of innate immune system receptors drives inflammaging, that is ameliorated by dietary restriction intervention [ATAC-seq]

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Stat1 activation, through systemic interferon signaling, and upregulation of innate immune system receptors drives inflammaging, that is ameliorated by dietary restriction intervention

Project description:Stat1 activation, through systemic interferon signaling, and upregulation of innate immune system receptors drives inflammaging, that is ameliorated by dietary restriction intervention

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Stat1 activation, through systemic interferon signaling, and upregulation of innate immune system receptors drives inflammaging, that is ameliorated by dietary restriction intervention [RNA-seq]

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Stat1 activation, through systemic interferon signaling, and upregulation of innate immune system receptors drives inflammaging, that is ameliorated by dietary restriction intervention

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

2022-08-25 | GSE162803 | GEO

Aged intestinal stem cells propagate cell-intrinsic sources of inflammaging in mice [ATAC_invivo]

Project description:Low-grade chronic inflammation is considered a hallmark of ageing and associated with impaired tissue function and development of disease. However, how cell-intrinsic and -extrinsic factors interact to establish this phenotype, termed inflammaging, remains poorly understood. We addressed this question in the mouse intestinal epithelium, using organoid cultures to dissect stem cell-intrinsic and -extrinsic sources of increased inflammatory signaling upon ageing. At the single-cell level, we found that inflammaging establishes differently in cells along the crypt-villus axis, including intestinal stem cells (ISCs). Importantly, the inflammaging phenotype was stably propagated by aged ISCs in organoid cultures and associated with increased chromatin accessibility of inflammation-associated loci in vivo and ex vivo, indicating a cell-intrinsic memory of inflammation. Mechanistically, we show that expression of inflammaging genes is dependent on STAT1 signaling. Together, our data reveal that inflammaging in the intestine is promoted by a cell-intrinsic mechanism, stably propagated by ISCs and associated with a disbalance in immune homeostasis.

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