Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

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

PROVIDER: PRJNA417573 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

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

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

| PRJNA417575 | ENA

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)

| PRJNA417572 | ENA

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

Project description: Not available

| S-EPMC6055154 | biostudies-literature

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.

2018-07-05 | GSE106669 | GEO

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.

2018-07-05 | GSE106666 | GEO

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.

2021-03-22 | PXD024356 | Pride

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

Project description:Rett syndrome is a severe neurodevelopmental disorder caused by loss-of-function mutations in the methyl-CpG-binding protein gene, MECP2. MeCP2 is a methyl-cytosine binding protein that is proposed to function as a transcriptional repressor. However, multiple gene expression studies comparing wild-type and MeCP2-deficient neurons have failed to identify gene expression changes consistent with loss of a classical transcriptional repressor. Recent work suggests that one function of MeCP2 in neurons is to temper the expression of the longest genes in the genome by binding to methylated CA dinucleotides (mCA) within transcribed regions of these genes. In the present study, we explore the mechanism of mCA and MeCP2 in fine-tuning the expression of long genes. We find that mCA is not only highly enriched within the body of genes normally repressed by MeCP2, but also enriched within extended megabase-scale regions surrounding MeCP2-repressed genes. While enrichment of mCA exists in a broad region around these genes, mCA within gene bodies appears to be the primary driver of gene repression by MeCP2. Disruption of methylation at CA sites within the brain results in depletion of MeCP2 across genes that normally contain a high density of gene-body mCA. We further find that the degree of gene repression by MeCP2 is proportional to the total number of methylated cytosine MeCP2 binding sites across the body of a gene. These findings suggest a model in which MeCP2 tunes gene expression in neurons by binding within the transcribed regions of genes to impede the elongation of RNA polymerase.

2016-12-01 | GSE90704 | 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.

2023-10-26 | GSE233898 | GEO