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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE182044 | 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 [myeloid cells]

Project description: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.

2021-11-19 | GSE181894 | 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

Wild type and EGR2 knock-out mouse alveolar macrophages

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

2024-08-31 | GSE181087 | GEO

Impairment of tissue repair in pneumonia due to β-cell deficiency: role of endoplasmic reticulum stress in alveolar macrophages.

Project description:ObjectiveDiabetes mellitus (DM) patients are susceptible to delayed resolution of pneumonia. However, the pathogenesis of the impaired tissue repair in inflamed lungs in diabetic patients is unknown. We evaluated phagocytosis of apoptotic cells (efferocytosis), hepatocyte growth factor (HGF) production in bronchoalveolar lavage fluid (BALF), and lung histology in the resolution phase following acute lung injury in streptozotocin (STZ)-induced β-cell-depleted hyperglycemic mice. We also investigated efferocytosis and HGF production by macrophages under β-cell depletion condition ex vivo.ResultsIn β-cell-depleted mice, efferocytosis was not significantly different from that in control mice; however, the concentration of HGF in BALF was decreased. In addition, diminished HGF production by alveolar macrophages and DNA synthesis in the alveolar epithelium was observed by immunohistochemistry. Ex vivo experiments confirmed that HGF production by macrophages was impaired under β-cell depletion probably because of endoplasmic reticulum stress.

| S-EPMC6431046 | biostudies-literature

Sex-specific adipose tissue imprinting of regulatory T cells.

Project description:Adipose tissue is an energy store and a dynamic endocrine organ1,2. In particular, visceral adipose tissue (VAT) is critical for the regulation of systemic metabolism3,4. Impaired VAT function-for example, in obesity-is associated with insulin resistance and type 2 diabetes5,6. Regulatory T (Treg) cells that express the transcription factor FOXP3 are critical for limiting immune responses and suppressing tissue inflammation, including in the VAT7-9. Here we uncover pronounced sexual dimorphism in Treg cells in the VAT. Male VAT was enriched for Treg cells compared with female VAT, and Treg cells from male VAT were markedly different from their female counterparts in phenotype, transcriptional landscape and chromatin accessibility. Heightened inflammation in the male VAT facilitated the recruitment of Treg cells via the CCL2-CCR2 axis. Androgen regulated the differentiation of a unique IL-33-producing stromal cell population specific to the male VAT, which paralleled the local expansion of Treg cells. Sex hormones also regulated VAT inflammation, which shaped the transcriptional landscape of VAT-resident Treg cells in a BLIMP1 transcription factor-dependent manner. Overall, we find that sex-specific differences in Treg cells from VAT are determined by the tissue niche in a sex-hormone-dependent manner to limit adipose tissue inflammation.

| S-EPMC7241647 | biostudies-literature

Transcript- and tissue-specific imprinting of a tumour suppressor gene.

Project description:The Bladder Cancer-Associated Protein gene (BLCAP; previously BC10) is a tumour suppressor that limits cell proliferation and stimulates apoptosis. BLCAP protein or message are downregulated or absent in a variety of human cancers. In mouse and human, the first intron of Blcap/BLCAP contains the distinct Neuronatin (Nnat/NNAT) gene. Nnat is an imprinted gene that is exclusively expressed from the paternally inherited allele. Previous studies found no evidence for imprinting of Blcap in mouse or human. Here we show that Blcap is imprinted in mouse and human brain, but not in other mouse tissues. Moreover, Blcap produces multiple distinct transcripts that exhibit reciprocal allele-specific expression in both mouse and human. We propose that the tissue-specific imprinting of Blcap is due to the particularly high transcriptional activity of Nnat in brain, as has been suggested previously for the similarly organized and imprinted murine Commd1/U2af1-rs1 locus. For Commd1/U2af1-rs1, we show that it too produces distinct transcript variants with reciprocal allele-specific expression. The imprinted expression of BLCAP and its interplay with NNAT at the transcriptional level may be relevant to human carcinogenesis.

| S-EPMC2666296 | biostudies-literature

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