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TNF promotes SREBP activity to regulate macrophage polarization and tissue repair [scRNA-seq]

ABSTRACT: TNF promotes SREBP activity to regulate macrophage polarization and tissue repair [scRNA-seq]

PROVIDER: PRJNA530558 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8837500.fastq.gz	Fastqsanger.gz
	SRR8837510.fastq.gz	Fastqsanger.gz
	SRR8837491.fastq.gz	Fastqsanger.gz
	SRR8837501.fastq.gz	Fastqsanger.gz
	SRR8837511.fastq.gz	Fastqsanger.gz

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TNF promotes SREBP activity to regulate macrophage polarization and tissue repair [ChIP-seq]

Project description:TNF-mediated macrophage polarization is important for inflammatory disease pathogenesis, but mechanisms that regulate polarization are not well understood. Transcriptomic and epigenomic analysis of the TNF response in primary human macrophages revealed late phase activation of SREBP2, the master regulator of cholesterol biosynthesis genes. TNF stimulation extended the genomic profile of SREBP2 occupancy to include binding to and activation of inflammatory and interferon response genes independently of its functions in sterol metabolism. Genetic ablation of SREBP function shifted the balance of macrophage polarization from M1 to an M2-like reparative phenotype in peritonitis and skin wound healing models. Genetic ablation of SREBP activity in myeloid cells or topical pharmacological inhibition of SREBP improved skin wound healing under homeostatic and chronic inflammatory conditions. Our results identify a new function and mechanism of action for SREBP2 in augmenting TNF-induced M1 macrophage polarization and inflammation, and open therapeutic avenues for promoting wound repair.

2019-04-03 | GSE129202 | GEO

TNF promotes SREBP activity to regulate macrophage polarization and tissue repair [scRNA-seq]

2019-04-03 | GSE129225 | GEO

TNF promotes SREBP activity to regulate macrophage polarization and tissue repair [RNA-seq]

2019-04-03 | GSE129210 | GEO

TNF promotes SREBP activity to regulate macrophage polarization and tissue repair [ATAC-seq]

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TNF promotes SREBP activity to regulate macrophage polarization and tissue repair

Project description:TNF promotes SREBP activity to regulate macrophage polarization and tissue repair

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TNF promotes SREBP activity to regulate macrophage polarization and tissue repair [ATAC-seq]

Project description:TNF promotes SREBP activity to regulate macrophage polarization and tissue repair [ATAC-seq]

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TNF promotes SREBP activity to regulate macrophage polarization and tissue repair [RNA-seq]

Project description:TNF promotes SREBP activity to regulate macrophage polarization and tissue repair [RNA-seq]

| PRJNA530534 | ENA

TNF promotes SREBP activity to regulate macrophage polarization and tissue repair [ChIP-seq]

Project description:TNF promotes SREBP activity to regulate macrophage polarization and tissue repair [ChIP-seq]

| PRJNA530522 | ENA

TNF promotes SREBP activity to regulate macrophage polarization and tissue repair

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

2019-04-03 | GSE129229 | GEO

Thrombocytes-derived Dickkopf1 promotes wound-healing macrophage polarization

Project description:Immune responses are crucial to maintaining tissue homeostasis upon tissue injury. Upon various types of challenges, macrophages play a central role in regulating inflammation and tissue repair processes. While an immunomodulatory role of Wnt antagonist Dickkopf1 (DKK1) has been implicated, the role of Wnt antagonist DKK1 in regulating macrophage polarization in inflammation and the tissue repair process remains elusive. Here we found that DKK1 induces differential gene expression profiles from type 2-cytokine-activated macrophages to promote inflammation and tissue repair. Importantly, DKK1 induced pro-inflammatory and pro-resolving gene expressions via JNK (c-jun N-terminal kinase) in macrophages. Furthermore, DKK1 potentiated IL-13-mediated macrophage polarization and activation. Co-inhibition of JNK and STAT6 markedly decreased pro-inflammatory and pro-resolving gene expressions by DKK1 and IL-13. Interestingly, thrombocyte-specific deletion of DKK1 in mice reduced monocyte-derived macrophages in the acute sterile bleomycin (BLM)-induced lung injury model, suggesting that thrombocytes communicate with macrophages via DKK1 to orchestrate inflammation-induced injury repair process. Taken together, our study demonstrates DKK1’s role as a key regulatory role in macrophage polarization in the injury-induced inflammation and repair process.

2023-12-06 | GSE247398 | GEO

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