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Repression of Human and Mouse Brain Inflammaging Transcriptome by Broad Gene Body Histone Hyperacetylation

ABSTRACT: Repression of Human and Mouse Brain Inflammaging Transcriptome by Broad Gene Body Histone Hyperacetylation

PROVIDER: PRJNA417575 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6267290.fastq.gz	Fastqsanger.gz
	SRR6267300_1.fastq.gz	Fastqsanger.gz
	SRR6267300_2.fastq.gz	Fastqsanger.gz
	SRR6267310_1.fastq.gz	Fastqsanger.gz
	SRR6267310_2.fastq.gz	Fastqsanger.gz

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Repression of Human and Mouse Brain Inflammaging Transcriptome by Broad Gene Body Histone Hyperacetylation (RNA-seq)

Project description:Repression of Human and Mouse Brain Inflammaging Transcriptome by Broad Gene Body Histone Hyperacetylation (RNA-seq)

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Repression of Human and Mouse Brain Inflammaging Transcriptome by Broad Gene Body Histone Hyperacetylation (ChIP-seq)

Project description:Repression of Human and Mouse Brain Inflammaging Transcriptome by Broad Gene Body Histone Hyperacetylation (ChIP-seq)

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Repression of human and mouse brain inflammaging transcriptome by broad gene-body histone hyperacetylation.

Project description:Brain "inflammaging," a low-grade and chronic inflammation, is a major hallmark for aging-related neurodegenerative diseases. Here, by profiling H3K27ac and gene expression patterns in human and mouse brains, we found that age-related up-regulated (Age-Up) and down-regulated (Age-Down) genes have distinct H3K27ac patterns. Although both groups show promoter H3K27ac, the Age-Up genes, enriched for inflammation-related functions, are additionally marked by broad H3K27ac distribution over their gene bodies, which is progressively reduced during aging. Age-related gene expression changes can be predicted by gene-body H3K27ac level. Contrary to the presumed transcription activation function of promoter H3K27ac, we found that broad gene-body hyper H3K27ac suppresses overexpression of inflammaging genes. Altogether, our findings revealed opposite regulations by H3K27ac of Age-Up and Age-Down genes and a mode of broad gene-body H3K27ac in repressing transcription.

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Repression of Human and Mouse Brain Inflammaging Transcriptome by Broad Gene Body Histone Hyperacetylation

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

2018-07-04 | GSE106670 | GEO

Repression of Human and Mouse Brain Inflammaging Transcriptome by Broad Gene Body Histone Hyperacetylation (RNA-seq)

Project description:RNA-seq data of human prefrontal cortex and mouse brain during aging and/or SAHA treatment were generated.

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Repression of Human and Mouse Brain Inflammaging Transcriptome by Broad Gene Body Histone Hyperacetylation (ChIP-seq)

Project description:ChIP-seq data of human prefrontal cortex and mouse brain during aging and/or SAHA treatment were generated.

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Organ-specific inflammaging in mice

Project description:Aging is accompanied by chronic, low-grade systemic inflammation, termed inflammaging, a main driver of age-associated diseases. Such sterile inflammation is typically characterized by elevated levels of pro-inflammatory mediators, such as cytokines and reactive oxygen species causing organ damage. Lipid mediators play important roles in the fine-tuning of both the promotion and the resolution of inflammation. Yet, it remains unclear how lipid mediators fit within the concept of inflammaging and how their biosynthesis and function is affected by aging. Here, we provide comprehensive signature profiles of inflammatory markers in organs afflicted with inflammation of young and old C57BL/6 mice. We reveal an organ-specific footprint of inflammation-related cytokines, chemokines and lipid mediators, which are distinctively affected by aging. While some organs are characterized by a pronounced pro-inflammatory microenvironment and impaired resolution during aging, others display elevated levels of pro-resolving mediators or an overall decrease in inflammatory signaling. Our results demonstrate that it proves difficult to establish a unifying concept for alterations of immunomodulatory mediators as consequence of aging and that organ specificity needs to be considered. Moreover, our data imply that inclusion of lipid mediators into the concept of inflammaging provides a comprehensive tool to characterize the inflammatory microenvironment during aging on a broader and yet, more detailed scope.

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DNA methylation in the gene body influences MeCP2-mediated gene repression

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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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