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

ABSTRACT: We profile the transcriptomes of over 3,000 mouse single myeloid cells from mouse lung to define the transcriptional profiles of monocytes and subsets of dendritic cells and macrophages. We perform differential gene expression analysis to determine the transcriptional regulators unique to each cluster.

ORGANISM(S): Mus musculus

PROVIDER: GSE181894 | GEO | 2021/11/19

REPOSITORIES: GEO

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

Project description:Alveolar macrophages are the most abundant macrophages in the healthy lung where they play key roles in homeostasis and immune surveillance against airborne pathogens. Tissue-specific differentiation and survival of alveolar macrophages rely on niche-derived factors, such as granulocyte-macrophage colony-stimulating factor (GM-CSF) and transforming growth factor–β (TGF-β). However, the nature of the downstream molecular pathways that regulate the identity and function of alveolar macrophages and their response to injury remain poorly understood. Here, we identify that the transcription factor EGR2 is an evolutionarily conserved feature of lung alveolar macrophages and show that cell-intrinsic EGR2 is indispensable for the tissue-specific identity of alveolar macrophages. Mechanistically, we show that EGR2 is driven by TGF-β and GM-CSF in a PPAR-γ–dependent manner to control alveolar macrophage differentiation. Functionally, EGR2 was dispensable for the regulation of lipids in the airways but crucial for the effective handling of the respiratory pathogen Streptococcus pneumoniae. Last, we show that EGR2 is required for repopulation of the alveolar niche after sterile, bleomycin-induced lung injury and demonstrate that EGR2-dependent, monocyte-derived alveolar macrophages are vital for effective tissue repair after injury. Collectively, we demonstrate that EGR2 is an indispensable component of the transcriptional network controlling the identity and function of alveolar macrophages in health and disease.

| S-EPMC7612216 | biostudies-literature

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

Project description:We compare the transcriptional profile of Egr2-sufficient or Egr2-deficient airway macrophages obtained from Lyz2-Cre-Egr2-floxed mice

2021-11-19 | GSE182043 | GEO

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

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

2021-11-19 | GSE182044 | GEO

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

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

| PRJNA754364 | ENA

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

Project description:The transcription factor EGR2 is indispensable for tissue-specific imprinting of alveolar macrophages in health and tissue repair

| PRJNA754360 | ENA

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

Project description:The transcription factor EGR2 is indispensable for tissue-specific imprinting of alveolar macrophages in health and tissue repair [myeloid cells]

| PRJNA753819 | ENA

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.

2024-08-29 | GSE181085 | GEO

CUT&RUN 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, 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.

2024-08-29 | GSE202858 | GEO

Wild type and EGR2 knock-out mouse alveolar macrophages

Project description:Wild type and EGR2 knock-out mouse alveolar macrophages

| PRJNA750652 | ENA

DNA repair is indispensable for survival after acute inflammation.

Project description:More than 15% of cancer deaths worldwide are associated with underlying infections or inflammatory conditions, therefore understanding how inflammation contributes to cancer etiology is important for both cancer prevention and treatment. Inflamed tissues are known to harbor elevated etheno-base (?-base) DNA lesions induced by the lipid peroxidation that is stimulated by reactive oxygen and nitrogen species (RONS) released from activated neutrophils and macrophages. Inflammation contributes to carcinogenesis in part via RONS-induced cytotoxic and mutagenic DNA lesions, including ?-base lesions. The mouse alkyl adenine DNA glycosylase (AAG, also known as MPG) recognizes such base lesions, thus protecting against inflammation-associated colon cancer. Two other DNA repair enzymes are known to repair ?-base lesions, namely ALKBH2 and ALKBH3; thus, we sought to determine whether these DNA dioxygenase enzymes could protect against chronic inflammation-mediated colon carcinogenesis. Using established chemically induced colitis and colon cancer models in mice, we show here that ALKBH2 and ALKBH3 provide cancer protection similar to that of the DNA glycosylase AAG. Moreover, Alkbh2 and Alkbh3 each display apparent epistasis with Aag. Surprisingly, deficiency in all 3 DNA repair enzymes confers a massively synergistic phenotype, such that animals lacking all 3 DNA repair enzymes cannot survive even a single bout of chemically induced colitis.

| S-EPMC3386829 | biostudies-other

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