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

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

PROVIDER: PRJNA556674 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11833509.fastq.gz	Fastqsanger.gz
	SRR11833510.fastq.gz	Fastqsanger.gz
	SRR11833511.fastq.gz	Fastqsanger.gz
	SRR11833512.fastq.gz	Fastqsanger.gz
	SRR9834210.fastq.gz	Fastqsanger.gz

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Similar Datasets

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

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

Adipose Tissue Macrophage Accrual in Obesity

Project description:Adipose Tissue Macrophage Accrual in Obesity

| PRJNA634570 | ENA

Perivascular Mesenchymal Cells Control Adipose Tissue Macrophage Accrual in Obesity

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

| PRJNA634571 | ENA

Adipose Tissue Macrophage Accrual in Obesity

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

2020-09-01 | GSE151093 | GEO

Perivascular mesenchymal cells control adipose-tissue macrophage accrual in obesity.

Project description:Chronic low-grade white adipose tissue (WAT) inflammation is a hallmark of metabolic syndrome in obesity. Here, we demonstrate that a subpopulation of mouse WAT perivascular (PDGFRβ+) cells, termed fibro-inflammatory progenitors (FIPs), activate proinflammatory signalling cascades shortly after the onset of high-fat diet feeding and regulate proinflammatory macrophage accumulation in WAT in a TLR4-dependent manner. FIPs activation in obesity is mediated by the downregulation of zinc-finger protein 423 (ZFP423), identified here as a transcriptional corepressor of NF-κB. ZFP423 suppresses the DNA-binding capacity of the p65 subunit of NF-κB by inducing a p300-to-NuRD coregulator switch. Doxycycline-inducible expression of Zfp423 in PDGFRβ+ cells suppresses inflammatory signalling in FIPs and attenuates metabolic inflammation of visceral WAT in obesity. Inducible inactivation of Zfp423 in PDGFRβ+ 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 NF-κB signalling.

| S-EPMC7669663 | biostudies-literature

ZFP423 Controls EBF2 Co-activator Recruitment and PPARgamma Occupancy to Determine the Thermogenic Plasticity of Adipocytes_ChAP-seq

Project description:Energy-storing white adipocytes maintain their identity by suppressing the gene program defining energy-burning thermogenic brown/beige adipocytes. Here, we reveal that the protein-protein interaction between the transcriptional co-regulator ZFP423 and brown/beige cell determination factor, EBF2, is essential for restraining the thermogenic phenotype of white adipose tissue (WAT). Disruption of the ZFP423-EBF2 protein interaction through CRISPR-Cas9 gene editing triggers widespread “browning” of WAT in adult mice. Mechanistically, adipocyte Zfp423 deficiency induces an EBF2 NuRD-to-BAF co-regulator switch and a shift in PPARgamma occupancy to thermogenic genes. This shift in PPARgamma occupancy increases the anti-diabetic efficacy of the PPARgamma agonist rosiglitazone in obesity while diminishing the unwanted weight-gaining effect of the drug. These data indicate that ZFP423 controls EBF2 co-activator recruitment and PPARgamma occupancy to determine the thermogenic plasticity of adipocytes and raise the concept of targeting transcriptional brakes in adipocyte gene expression as a therapeutic strategy to induce thermogenic adipocyte biogenesis in obesity.

2022-05-01 | GSE175653 | GEO

ZFP423 Controls EBF2 Co-activator Recruitment and PPARgamma Occupancy to Determine the Thermogenic Plasticity of Adipocytes_ChIP-seq

2022-05-01 | GSE175654 | GEO

Identification of Zfp423-dependent genes in adult inguinal white adipocytes

Project description:We derived a model that allows for doxycycline-inducible deletion of Zfp423 in mature adipocytes of adult mice (Adiponectin-rtTA; TRE-CRE; Zfp423 loxP/loxP). In these animals deletion of Zfp423 results in a spontaneous conversion of white adipocytes into beige-like adipocytes at room temperature. The goal of this expression analysis was to 1) determine the gene programs dependent on adipocyte Zfp423 in inguinal WAT, and 2) determine the similarity between the converted beige-like cells to normal beige adipose tissue that accumulates upon cold exppsure.

2016-02-10 | GSE74899 | GEO

Identification of genes characteristic of Zfp423-expressing perivascular cells in mouse epididymal adipose tissue

Project description:Committed perivascular preadipocytes were genetically labelled in transgenic mice expressing GFP under the control of the locus (BAC) for Zfp423, a gene controlling preadipocyte determination. The overall goal was to identify genes differentially expressed between perivascular (PDGFRbeta+) GFP+ cells and perivascualar (PDGFRbeta+) GFP- cells from mouse epididymal adipose tissue.

2015-10-01 | GSE70789 | GEO

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