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Chromatin Remodeling Drives Immune-Fibroblast Cell Communication in Heart Failure (ChIP-Seq)

ABSTRACT: Chromatin Remodeling Drives Immune-Fibroblast Cell Communication in Heart Failure (ChIP-Seq)

PROVIDER: PRJNA915382 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22882100.fastq.gz	Fastqsanger.gz
	SRR22882101.fastq.gz	Fastqsanger.gz
	SRR22882102.fastq.gz	Fastqsanger.gz
	SRR22882103.fastq.gz	Fastqsanger.gz
	SRR22882104.fastq.gz	Fastqsanger.gz

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Chromatin Remodeling Drives Immune-Fibroblast Cell Communication in Heart Failure

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Chromatin Remodeling Drives Immune-Fibroblast Cell Communication in Heart Failure (scRNA-Seq)

Project description:Chronic inflammation and tissue fibrosis are common stress responses that worsen organ function, yet their crosstalk is poorly understood. Here, we show that conditional deletion of the transcription co-activator Brd4 in Cx3cr1-positive myeloid cells ameliorates heart failure and is associated with a dramatic reduction in fibroblast activation. We identified a specific BRD4-occupied enhancer in Cx3cr1-positive cells that controls expression of Interleukin-1 beta (Il1b), and show that secreted IL1B activates a p65/RELA-dependent enhancer downstream of MEOX1, driving a profibrotic response in human cardiac fibroblasts. In vivo, antibody-mediated IL1B neutralization prevented stress-induced expression of MEOX1, inhibited fibroblast activation, and improved cardiac function in heart failure. The elucidation of BRD4-dependent crosstalk between a specific immune cell subset and fibroblasts through IL1B provides new therapeutic strategies for heart disease and other disorders of chronic inflammation and maladaptive tissue remodeling.

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Chromatin Remodeling Drives Immune-Fibroblast Cell Communication in Heart Failure (ChIP-Seq)

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