Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Adipose Tissue Macrophage Accrual in Obesity

ABSTRACT: Adipose Tissue Macrophage Accrual in Obesity

PROVIDER: PRJNA634570 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR11833509.fastq.gz	Fastqsanger.gz
	SRR11833510.fastq.gz	Fastqsanger.gz
	SRR11833511.fastq.gz	Fastqsanger.gz
	SRR11833512.fastq.gz	Fastqsanger.gz
	SRR11833513.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 28

Similar Datasets

Perivascular Mesenchymal Cells Control Adipose Tissue Macrophage Accrual in Obesity

Project description:Chronic low-grade visceral white adipose tissue (WAT) inflammation is a hallmark of metabolic syndrome in obesity. Here, we demonstrate that a subpopulation of adipose tissue perivascular (PDGFRb+) cells, termed “fibro-inflammatory progenitors” (FIPs), activate pro-inflammatory signaling cascades shortly after the onset of high-fat diet feeding of mice and regulate pro-inflammatory macrophage accumulation in WAT in a TLR4-dependent manner. FIPs activation in obesity is mediated by the downregulation of ZFP423, identified here as a transcriptional co-regulator of NFkB. Biochemical analysis of ZFP423-protein complexes and ChIP-seq analysis reveal that ZFP423 suppresses the DNA-binding capacity of the p65 subunit of NFkB by inducing a p300 to NuRD co-regulator switch. Doxycycline-inducible expression of Zfp423 in PDGFRb+ cells suppresses inflammatory signaling in FIPs and attenuates metabolic inflammation of visceral WAT in obesity. Inducible inactivation of Zfp423 in PDGFRb+ cells increases FIP activity, exacerbates adipose macrophage accrual, and promotes WAT dysfunction. These studies implicate perivascular mesenchymal cells as important regulators of chronic adipose tissue inflammation in obesity and identify ZFP423 as a transcriptional break on NFkB signaling.

2020-09-01 | GSE151092 | GEO

Perivascular Mesenchymal Cells Control Adipose Tissue Macrophage Accrual in Obesity

Project description:Perivascular Mesenchymal Cells Control Adipose Tissue Macrophage Accrual in Obesity

| PRJNA634571 | ENA

Mural Cell ZFP423 Controls Adipose Tissue Macrophage Accrual in Obesity [ChIP-seq]

Project description:Chronic low-grade visceral white adipose tissue (WAT) inflammation is a hallmark of metabolic syndrome in obesity. Here, we demonstrate that a specific subpopulation of adipose tissue perivascular (PDGFRb+) stromal cells, termed “fibro-inflammatory progenitors” (FIPs), activate pro-inflammatory signaling cascades shortly after the onset of high-fat diet feeding of mice and control the accumulation of pro-inflammatory macrophages in WAT. The activation of FIPs is mediated by the downregulation of ZFP423, identified here as a transcriptional co-regulator of NFkB. Biochemical analysis of ZFP423-protein complexes and ChIP-seq analysis reveal that ZFP423 suppresses the DNA-binding capacity of the p65 subunit of NFkB by inducing a co-regulator switch. Doxycycline-inducible expression of Zfp423 in PDGFRb+ cells suppresses inflammatory signaling in FIPs and attenuates macrophage accumulation within visceral WAT of obese mice. Conversely, inducible inactivation of Zfp423 in PDGFRb+ cells increases FIP activity, exacerbates adipose macrophage accrual, and promotes WAT dysfunction in obese mice. These studies implicate mural cells as sentinels and gatekeepers of adipose tissue inflammation in obesity.

2020-09-01 | GSE134868 | GEO

Mural Cell ZFP423 Controls Adipose Tissue Macrophage Accrual in Obesity [ChIP-seq]

Project description:Mural Cell ZFP423 Controls Adipose Tissue Macrophage Accrual in Obesity [ChIP-seq]

| PRJNA556674 | ENA

RNA-seq of human adipose tissue macrophage subtypes in obesity

Project description:RNA-seq of human adipose tissue macrophage subtypes in obesity

| PRJNA784780 | ENA

Influenza Infection Promotes Lung Accrual of Macrophages with an Obese Adipose Tissue Transcriptomic Signature

Project description:Obesity is a risk factor for increased lung damage and disease severity during influenza virus infection. White adipose tissue (WAT) inflammation is a key driver of disease pathogenesis in obesity. While lung tissue immune cell pathogenic mechanisms are dogmatically studied in influenza virus infection, how obesity modifies lung and WAT immune cell character and contribution to amplify disease severity remains unknown. We show that obesity results in lung immune cells having a more inflammatory transcriptome in response to influenza infection than in the lean state. Further, in both lean and obese mice, influenza virus infection induces expression of inflammatory genes in visceral WAT and dominantly modifies the WAT immune cell milieu in obesity. Notably, obese influenza virus-infected mice exhibit a decrease in white adipose tissue macrophage (ATM) populations that inversely correlates with the increase in infiltrating lung macrophage numbers.

2025-02-26 | GSE266326 | GEO

Adipose Tissue Omics In Obesity

Project description:Adipose Tissue Omics In Obesity

| PRJNA1006496 | ENA

Adipose Tissue Omics In Obesity

Project description:Adipose Tissue Omics In Obesity

| PRJNA1006463 | ENA

Visceral adipose tissue macrophage subsets

Project description:Visceral adipose tissue macrophage subsets

| PRJNA484897 | ENA

Adipose Tissue Macrophage Accrual in Obesity

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