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HDAC3 requirement for the inflammatory gene expression program in macrophages

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

ORGANISM(S): Mus musculus

PROVIDER: GSE33164 | GEO | 2012/07/09

SECONDARY ACCESSION(S): PRJNA149173

REPOSITORIES: GEO

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HDAC3 requirement for the inflammatory gene expression program in macrophages

Project description:This SuperSeries is composed of the following subset Series: GSE33162: HDAC3 requirement for the inflammatory gene expression program in macrophages [gene expression] GSE33163: HDAC3 requirement for the inflammatory gene expression program in macrophages [ChIP_Seq] Refer to individual Series

2012-07-08 | E-GEOD-33164 | biostudies-arrayexpress

The study of inflammatory responses in mammalian macrophages with LPS stimulation

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-02-24 | E-GEOD-76563 | biostudies-arrayexpress

Dichotomous Engagement of HDAC3 Activity Governs Inflammatory Responses

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

2020-04-30 | GSE140611 | GEO

Requirement for the histone deacetylase Hdac3 for the inflammatory gene expression program in macrophages.

Project description:Histone deacetylases (HDACs) regulate inflammatory gene expression, as indicated by the potent antiinflammatory activity of pan-HDAC inhibitors. However, the specific contribution of each of the 11 HDAC proteins to the inflammatory gene expression program is unknown. Using an integrated genomic approach, we found that Hdac3-deficient macrophages were unable to activate almost half of the inflammatory gene expression program when stimulated with LPS. A large part of the activation defect was attributable to loss of basal and LPS-inducible expression of IFN-β, which maintains Stat1 protein levels in unstimulated cells and acts in an autocrine/paracrine manner after stimulation to promote a secondary wave of Stat1-dependent gene expression. Loss of Hdac3-mediated repression of nuclear receptors led to hyperacetylation of thousands of genomic sites and associated gene derepression. The up-regulation of the constitutively expressed prostaglandin endoperoxide synthase, Ptgs1 (Cox-1), a nuclear receptor target, had a causative role in the phenotype because its chemical inhibition reverted, albeit partially, the Ifn-β activation defect. These data indicate a central role for Hdac3 in inflammation and may have relevance for the use of selective Hdac inhibitors as antiinflammatory agents.

| S-EPMC3479529 | biostudies-literature

Gene expression profiles in mouse livers depleted of HDAC3 or NCOR1

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-11-25 | E-GEOD-49388 | biostudies-arrayexpress

HDAC3 requirement for the inflammatory gene expression program in macrophages [ChIP_Seq]

Project description:Pan-Hdac inhibitors (HDACi) are endowed with a potent anti-inflammatory activity, but the relative role of each of the eleven Hdac proteins sensitive to HDACi to the inflammatory gene expression program is unknown. Using an integrated genomic approach we found that Hdac3-deficient macrophages are unable to activate almost half of the inflammatory gene expression program when stimulated with lipopolysaccharide (LPS). A large part of the activation defect is due to loss of basal and LPS-inducible expression of IFNb, which in basal cells maintains Stat1 protein levels, and after stimulation acts in an autocrine/paracrine manner to promote a secondary wave of Stat1-dependent gene expression. We show that loss of Hdac3-mediated repression of nuclear receptors leads to hyperacetylation of thousands of genomic sites and associated gene derepression. The upregulation of the constitutively expressed prostaglandin endoperoxide synthase, Ptgs1 (Cox-1), has a causative role in the phenotype, since its chemical inhibition reverts the Ifnb activation defect. These data may have relevance for the use of selective Hdac inhibitors as anti-inflammatory agents. Chromatin immuno-precipitations of H4 histone pan-acetylation followed by multiparallel sequencing performed in murine bone marrow-derive macrophages. Experiments carried out in untreated cells as well as in cells treated for 4hrs with lipopolysaccharide (LPS), for both HDAC3 +/- (wt) and HDAC3 -/- (KO) mice.

2012-07-08 | E-GEOD-33163 | biostudies-arrayexpress

HDAC3 IS AN EPIGENETIC INHIBITOR OF THE CYTOTOXICITY PROGRAM IN CD8 T CELLS

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

2020-04-22 | GSE143644 | GEO

Hdac3 Interaction with p300 Histone Acetyltransferase Regulates the Oligodendrocyte and Astrocyte Lineage Fate Switch

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-02-21 | E-GEOD-76412 | biostudies-arrayexpress

HDAC3 requirement for the inflammatory gene expression program in macrophages [gene expression]

Project description:Pan-Hdac inhibitors (HDACi) are endowed with a potent anti-inflammatory activity, but the relative role of each of the eleven Hdac proteins sensitive to HDACi to the inflammatory gene expression program is unknown. Using an integrated genomic approach we found that Hdac3-deficient macrophages are unable to activate almost half of the inflammatory gene expression program when stimulated with lipopolysaccharide (LPS). A large part of the activation defect is due to loss of basal and LPS-inducible expression of IFNb, which in basal cells maintains Stat1 protein levels, and after stimulation acts in an autocrine/paracrine manner to promote a secondary wave of Stat1-dependent gene expression. We show that loss of Hdac3-mediated repression of nuclear receptors leads to hyperacetylation of thousands of genomic sites and associated gene derepression. The upregulation of the constitutively expressed prostaglandin endoperoxide synthase, Ptgs1 (Cox-1), has a causative role in the phenotype, since its chemical inhibition reverts the Ifnb activation defect. These data may have relevance for the use of selective Hdac inhibitors as anti-inflammatory agents. Gene expression profiles for bone marrow-derived macrophages from either HDAC3 +/- (wt) or HDAC3 -/- (KO). Cells were left untreated or challenged with lipopolysaccharide (LPS) for 4hrs. Each genotype-treatment combination was performed in triplicate.

2012-07-08 | E-GEOD-33162 | biostudies-arrayexpress

HDAC3 requirement for the inflammatory gene expression program in macrophages [ChIP_Seq]

2012-07-09 | GSE33163 | GEO

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