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

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

PROVIDER: PRJNA779697 | ENA |

REPOSITORIES: ENA

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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 [RNA-Seq]

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

| PRJNA779695 | ENA

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 [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]

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 | GSE188613 | GEO

H3K27me3 regulates macrophage cytokine transcription and impacts on Collagen Induced Arthritis

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

2022-03-11 | GSE188616 | GEO

Transcription profiling of DBA/1J mouse with collagen induced arthritis

Project description:Time course of collagen-induced arthritis in DBA/1J male mice, synchronized on day 28 with 10ug LPS

2009-11-16 | E-TABM-661 | biostudies-arrayexpress

Collagen induced arthritis plasma proteomic analysis

Project description:The aim of the project is to analyze the plasma proteomic profile of an animal model of arthritis (Collagen Induced Arthritis; CIA) in response to different treatments. For this, plasma samples from mice under five different treatments were analyzed (N=6 per group): Vehicle, CIA, CIA + Δ9-THCA-A (20 mg / kg), CIA + Δ9-THCA-A (20 mg / kg) + T0070907 (5 mg / kg) and CIA + Δ9-THCA-A (20 mg / kg) + SR141716A (5 mg / kg).

2020-09-18 | PXD015274 | Pride

Transcriptomic analysis of synovial cells derived from collagen-induced arthritis mice

Project description:The destruction of bone and cartilage results in a loss of joint functionality, critically impairing the quality of life in arthritis patients. Synovial fibroblasts (SFs) critically contribute to the pathogenesis of rheumatoid arthritis (RA) by acquiring either a pro-inflammatory or tissue-destructive phenotype. To explore the molecular mechanisms underlying the pathogenic fibroblast phenotype in arthritis, we performed single-cell RNA sequencing (scRNA-seq) on the synovial cells which were isolated from collagen-induced arthritis (CIA) mice.

2022-07-06 | GSE192504 | GEO

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