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RNA-seq of human adipose tissue macrophage subtypes in obesity

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

PROVIDER: PRJNA784780 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17073222.fastq.gz	Fastqsanger.gz
	SRR17073223.fastq.gz	Fastqsanger.gz
	SRR17073224.fastq.gz	Fastqsanger.gz
	SRR17073225.fastq.gz	Fastqsanger.gz
	SRR17073226.fastq.gz	Fastqsanger.gz

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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.

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