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EGR2 is upregulated in monocyte-derived macrophages in MASH liver

ABSTRACT: EGR2 is upregulated in monocyte-derived macrophages in MASH liver

PROVIDER: PRJNA1100488 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28698571.fastq.gz	Fastqsanger.gz
	SRR28698572.fastq.gz	Fastqsanger.gz
	SRR28698573.fastq.gz	Fastqsanger.gz
	SRR28698574.fastq.gz	Fastqsanger.gz
	SRR28698575.fastq.gz	Fastqsanger.gz

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EGR2 is upregulated in monocyte-derived macrophages in MASH liver

Project description:This analysis was perfomed to explore the transcription factors that were enhanced in MASH liver macrophages.

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EGR2 is required for the acquisition of hLAM phenotype by monocyte-derived macrophages in MASH.

Project description:This analysis was performed to understand the difference between WT and EGR2 KO macrophages in MASH liver.

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EGR2 is required for the acquisition of hLAM phenotype by monocyte-derived macrophages in MASH.

Project description:EGR2 is required for the acquisition of hLAM phenotype by monocyte-derived macrophages in MASH.

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Lipid Associated Macrophages' Promotion of Fibrosis Resolution during MASH regression requires TREM2

Project description:While macrophage heterogeneity during Metabolic dysfunction-associated steatohepatitis (MASH) has been described, the fate of these macrophages during MASH regression is poorly understood. Comparing macrophage heterogeneity during MASH progression vs regression, we identified specific macrophage sub- populations that are critical for MASH/fibrosis resolution. We elucidated the restorative pathways and gene signatures that define regression associated macrophages (RAM) and establish the importance of TREM2+ macrophages during MASH regression. Liver resident Kupffer cells are lost during MASH and are replaced by four distinct monocyte derived macrophage sub-populations. Trem2 is expressed in two macrophage sub- populations: (i) monocyte-derived macrophages occupying the Kupffer cell niche (MoKC) and (ii) lipid-associated macrophages (LAM). In regression livers, no new transcriptionally distinct MF sub-population emerged. However, the relative macrophage composition changed during regression compared to MASH. While MoKC was the major macrophage sub-population during MASH, they decreased during regression. LAM was the dominant macrophage sub-type during MASH regression and maintained Trem2 expression. Both MoKC and LAM were enriched in disease resolving pathways. Absence of TREM2 restricted the emergence of LAMs and formation of hepatic crown like structures (hCLS). TREM2+ macrophages are functionally important not only for restricting MASH-fibrosis progression, but also for effective regression of inflammation and fibrosis. TREM2+ MF are superior collagen degraders. Lack of TREM2+ macrophages also prevented elimination of hepatic steatosis and inactivation of HSC during regression, indicating their significance in metabolic co-ordination with other cell- types in the liver. TREM2 imparts this protective effect through multifactorial mechanisms, including improved phagocytosis, lipid-handling and collagen degradation.

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Monocyte-derived Macrophages

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The transcription factor EGR2 is indispensable for tissue-specific imprinting of alveolar macrophages in health and tissue repair [Alveolar macrophages]

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ATAC-seq in wild type and EGR2 knock-out mouse alveolar macrophages

Project description:The alveolar macrophages (AMs) as a component of the innate immunity of the lung play important role in the elimination of inhaled microbes and harmful agents. The transcription factor EGR2 is a known marker transcription factor of AMs but its exact epigenetic and transcriptomic effects have not been examined. In our study, we performed ATAC-seq and RNA-seq in WT and EGR2 deficient alveolar macrophages to describe the mechanism of action and to predict potential direct target genes of EGR2. Clec7a is one of the targets of this transcription factor which is essential in the zymosan-induced inflammatory response. We further analyzed this process by applying in vivo mouse model. Our findings demonstrate that EGR2 is a key transcriptional activator, responsible for the intact protective program against different pathogens, especially fungi in AMs.

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Project description:The alveolar macrophages (AMs) as a component of the innate immunity of the lung play important role in the elimination of inhaled microbes and harmful agents. The transcription factor EGR2 is a known marker transcription factor of AMs but its exact epigenetic and transcriptomic effects have not been examined. In our study, we performed ATAC-seq, RNA-seq, and CUT&RUN in WT and EGR2 deficient alveolar macrophages to describe the mechanism of action and to predict potential direct target genes of EGR2. Clec7a is one of the targets of this transcription factor which is essential in the zymosan-induced inflammatory response. We further analyzed this process by applying in vivo mouse model. Our findings demonstrate that EGR2 is a key transcriptional activator, responsible for the intact protective program against different pathogens, especially fungi in AMs.

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