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H3K27me3 regulates macrophage cytokine transcription and impacts on Collagen Induced Arthritis

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

ORGANISM(S): Mus musculus

PROVIDER: GSE188616 | GEO | 2022/03/11

REPOSITORIES: GEO

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H3K27me3 regulates macrophage cytokine transcription and impacts on Collagen Induced Arthritis [ChIP-Seq]

Project description:The role of epigenetic regulation has been introduced in the process of macrophage polarization and the pathogenesis of inflammatory diseases. As a repressive epigenetic marker, tri-methylation of lysine 27 on histone H3 (H3K27me3) was shown to be important for transcriptional gene expression regulation. Here, we comprehensively analysed H3K27me3 binding promoter sequences by ChIP-seq and corresponding genes function by RNA sequencing in two differentially polarized macrophage populations. The results revealed that H3K27me3 binds on the promoter regions of multiple critical cytokine genes and suppressed their transcription, especially in M-CSF derived macrophages but not GM-CSF derived counterparts. The in vivo study results suggested that symptoms of collagen induced arthritis (CIA) mice can be relieved by reversing the loss of H3K27me3 and reducing IL6 parasecretion of macrophages, suggesting that H3K27me3 might act as a switch in the pathological processes of rheumatoid arthritis (RA). Our results may provide a new approach for the treatment of inflammatory and autoimmune disorders.

2024-11-09 | GSE188614 | GEO

H3K27me3 regulates macrophage cytokine transcription and impacts on Collagen Induced Arthritis [ATAC-Seq]

2024-11-09 | GSE188613 | GEO

H3K27me3 regulates macrophage cytokine transcription and impacts on Collagen Induced Arthritis [RNA-Seq]

Project description:The role of epigenetic regulation has been introduced in the process of macrophage polarization and the pathogenesis of inflammatory diseases. As a repressive epigenetic marker, tri-methylation of lysine 27 on histone H3 (H3K27me3) was shown to be important for transcriptional gene expression regulation. Here, we comprehensively analyzed H3K27me3 binding promoter sequences by ChIP-seq and corresponding genes function by RNA sequencing in two differentially polarized macrophage populations. The results revealed that H3K27me3 binds on the promoter regions of multiple critical cytokine genes and suppressed their transcription, especially in M-CSF derived macrophages but not GM-CSF derived counterparts. The in vivo study results suggested that symptoms of collagen induced arthritis (CIA) mice can be relieved by reversing the loss of H3K27me3 and reducing IL6 parasecretion of macrophages, suggesting that H3K27me3 might act as a switch in the pathological processes of rheumatoid arthritis (RA). Our results may provide a new approach for the treatment of inflammatory and autoimmune disorders.

2022-03-10 | GSE188615 | GEO

H3K27me3 regulates macrophage cytokine transcription and impacts on Collagen Induced Arthritis

Project description:H3K27me3 regulates macrophage cytokine transcription and impacts on Collagen Induced Arthritis

| PRJNA779693 | ENA

H3K27me3 regulates macrophage cytokine transcription and impacts on Collagen Induced Arthritis [ChIP-Seq]

Project description:H3K27me3 regulates macrophage cytokine transcription and impacts on Collagen Induced Arthritis [ChIP-Seq]

| PRJNA779696 | ENA

H3K27me3 regulates macrophage cytokine transcription and impacts on Collagen Induced Arthritis [ATAC-Seq]

Project description:H3K27me3 regulates macrophage cytokine transcription and impacts on Collagen Induced Arthritis [ATAC-Seq]

| PRJNA779697 | ENA

H3K27me3 regulates macrophage cytokine transcription and impacts on Collagen Induced Arthritis [RNA-Seq]

Project description:H3K27me3 regulates macrophage cytokine transcription and impacts on Collagen Induced Arthritis [RNA-Seq]

| PRJNA779695 | ENA

Diacylglycerol Kinase ? Regulates Macrophage Responses in Juvenile Arthritis and Cytokine Storm Syndrome Mouse Models.

Project description:Dysregulation of monocyte and macrophage responses are often observed in children with systemic juvenile idiopathic arthritis (sJIA) and cytokine storm syndrome (CSS), a potentially fatal complication of chronic rheumatic diseases. Both conditions are associated with activation of TLR signaling in monocyte and macrophage lineage cells, leading to overwhelming inflammatory responses. Despite the importance of TLR engagement in activating proinflammatory macrophages, relatively little is known about activation of intrinsic negative regulatory pathways to attenuate excessive inflammatory responses. In this study, we demonstrate that loss of diacylglycerol (DAG) kinase (Dgk) ?, an enzyme which converts DAG into phosphatidic acid, limits inflammatory cytokine production in an arthritic mouse model dependent on TLR2 signaling and in a CSS mouse model dependent on TLR9 signaling. In vitro, Dgk? deficiency results in reduced production of TNF-?, IL-6, and IL-1? and in limited M1 macrophage polarization. Mechanistically, Dgk? deficiency decreases STAT1 and STAT3 phosphorylation. Moreover, Dgk? levels are increased in macrophages derived from mice with CSS or exposed to plasma from sJIA patients with active disease. Our data suggest that Dgk? induction in arthritic conditions perpetuates systemic inflammatory responses mediated by macrophages and highlight a potential role of Dgk?-DAG/phosphatidic acid axis as a modulator of inflammatory cytokine production in sJIA and CSS.

| S-EPMC6920556 | biostudies-literature

Sperm-inherited H3K27me3 impacts offspring transcription and development in C. elegans.

Project description:Paternal epigenetic inheritance is gaining attention for its growing medical relevance. However, the form in which paternal epigenetic information is transmitted to offspring and how it influences offspring development remain poorly understood. Here we show that in C. elegans, sperm-inherited chromatin states transmitted to the primordial germ cells in offspring influence germline transcription and development. We show that sperm chromosomes inherited lacking the repressive histone modification H3K27me3 are maintained in that state by H3K36me3 antagonism. Inheritance of H3K27me3-lacking sperm chromosomes results in derepression in the germline of somatic genes, especially neuronal genes, predominantly from sperm-inherited alleles. This results in germ cells primed for losing their germ cell identity and adopting a neuronal fate. These data demonstrate that histone modifications are one mechanism through which epigenetic information from a father can shape offspring gene expression and development.

| S-EPMC6426959 | biostudies-literature

BTN2A2 protein negatively regulates T cells to ameliorate collagen-induced arthritis in mice.

Project description:Rheumatoid arthritis (RA) is an autoimmune disorder characterized by persistent inflammatory responses in target tissues and organs, resulting in the destruction of joints. Collagen type II (CII)-induced arthritis (CIA) is the most used animal model for human RA. Although BTN2A2 protein has been previously shown to inhibit T cell functions in vitro, its effect on autoimmune arthritis has not been reported. In this study, we investigate the ability of a recombinant BTN2A2-IgG2a Fc (BTN2A2-Ig) fusion protein to treat CIA. We show here that administration of BTN2A2-Ig attenuates established CIA, as compared with control Ig protein treatment. This is associated with reduced activation, proliferation and Th1/Th17 cytokine production of T cells in BTN2A2-Ig-treated CIA mice. BTN2A2-Ig also inhibits CII-specific T cell proliferation and Th1/Th17 cytokine production. Although the percentage of effector T cells is decreased in BTN2A2-Ig-treated CIA mice, the proportions of naive T cells and regulatory T cells is increased. Furthermore, BTN2A2-Ig reduces the percentage of proinflammatory M1 macrophages but increases the percentage of anti-inflammatory M2 macrophages in the CIA mice. Our results suggest that BTN2A2-Ig protein has the potential to be used in the treatment of collagen-induced arthritis models.

| S-EPMC8481265 | biostudies-literature

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