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Histone Deacetylase 3 is an Epigenomic Brake in Macrophage Alternative Activation (microarray)

ABSTRACT: Macrophages, a key cellular component of inflammation, become functionally polarized in a signal- and context-specific manner. Th2 cytokines such as IL-4 polarize macrophages to a state of alternative activation that limits inflammation and promotes wound healing. Alternative activation is mediated by a transcriptional program that is influenced by epigenomic modifications including histone acetylation. To determine if Histone Deacetylase 3 (HDAC3) has a role in macrophage polarization including alternative activation, we have performed global gene expression analysis in macrophages with and without HDAC3 and with or without IL-4 exposure. From this data, we conclude that macrophages lacking histone deacetylase 3 (HDAC3) display a polarization phenotype similar to IL-4 induced alternative activation and furthermore are hyper-responsive to IL-4 stimulation.

ORGANISM(S): Mus musculus

PROVIDER: GSE33608 | GEO | 2011/11/10

SECONDARY ACCESSION(S): PRJNA154329

REPOSITORIES: GEO

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Histone Deacetylase 3 is an Epigenomic Brake in Macrophage Alternative Activation (microarray)

Project description:Macrophages, a key cellular component of inflammation, become functionally polarized in a signal- and context-specific manner. Th2 cytokines such as IL-4 polarize macrophages to a state of alternative activation that limits inflammation and promotes wound healing. Alternative activation is mediated by a transcriptional program that is influenced by epigenomic modifications including histone acetylation. To determine if Histone Deacetylase 3 (HDAC3) has a role in macrophage polarization including alternative activation, we have performed global gene expression analysis in macrophages with and without HDAC3 and with or without IL-4 exposure. From this data, we conclude that macrophages lacking histone deacetylase 3 (HDAC3) display a polarization phenotype similar to IL-4 induced alternative activation and furthermore are hyper-responsive to IL-4 stimulation. Mouse bone marrow derived macrophages were obtained from both control and HDAC3 KO animals and treated with vehicle control (BSA) or IL-4 for 24 hours. RNA was isolated and subjected to analysis using an Agilent Whole Genome Microarray Kit.

2011-11-10 | E-GEOD-33608 | biostudies-arrayexpress

Histone Deacetylase 3 is an Epigenomic Brake in Macrophage Alternative Activation (ChIP-Seq)

Project description:We report the genomic regions enriched in Histone Deacetylase 3 (HDAC3) in mouse bone marrow derived macrophages. Furthermore, we also report the genomic acetylation pattern on Histone 3, Lysine 9 (H3K9) in macrophages with and without HDAC3 and/or treated with Th2 cytokine IL-4. HDAC3 enriched genomic regions in mouse bone marrow dervied macrophages and H3K9Ac enriched genomic regions in wild-type macrophages and macrophages treated with IL-4 and/or deficient in HDAC3.

2011-11-10 | E-GEOD-33596 | biostudies-arrayexpress

Histone Deacetylase 3 is an Epigenomic Brake in Macrophage Alternative Activation (ChIP-Seq)

2011-11-10 | GSE33596 | GEO

Histone Deacetylase 3 is an Epigenomic Brake in Macropahge Alternative Activation

Project description:This SuperSeries is composed of the following subset Series: GSE33596: Histone Deacetylase 3 is an Epigenomic Brake in Macrophage Alternative Activation (ChIP-Seq) GSE33608: Histone Deacetylase 3 is an Epigenomic Brake in Macrophage Alternative Activation (microarray) Refer to individual Series

2011-11-10 | E-GEOD-33609 | biostudies-arrayexpress

The transcription factor EGR2 is the molecular linchpin connecting STAT6 activation to the stable epigenomic program of alternative macrophage polarization

Project description:Macrophages polarize into functionally distinct subtypes while responding to microenvironmental cues. The identity of proximal transcription factors (TFs) downstream of the polarization signals are known, but their activity is typically transient, failing to explain the long-term, stable epigenomic programs developed. Here, we mapped the early and late epigenomic changes of interleukin-4 (IL-4)-induced alternative macrophage polarization. We identified the TF, Early Growth Response 2 (EGR2), bridging the early-transient and late-stable gene expression program of polarization. EGR2 is a direct target of IL-4-activated STAT6, having broad action indispensable for 77% of the induced gene signature of alternative polarization, including its autoregulation and a robust, downstream TF cascade involving PPARG. Mechanistically, EGR2 binding results in chromatin opening and the recruitment of chromatin remodelers and RNA-polymerase II. Egr2 induction is evolutionarily conserved during alternative polarization of mouse and human macrophages. In the context of tissue resident macrophages, Egr2 expression is most prominent in the lung of a variety of species. Thus, EGR2 is an example of an essential and evolutionarily conserved broad acting factor, linking transient polarization signals to stable epigenomic and transcriptional changes in macrophages.

2020-09-15 | GSE151015 | GEO

IFN-γ and IL-4 regulate epigenetic modifiers in macrophages

Project description:Interferon-γ (IFN-γ) or interleukin-4 (IL-4) prime macrophages towards classical (M1) or alternative (M2) activation, respectively. How IFN-γ and IL-4 prime epigenetic responses by altering expression of histone modifying enzymes and how this affects M1/M2 polarization is incompletely understood.

2017-01-15 | GSE83957 | GEO

Histone Deacetylase 3 is an Epigenomic Brake in Macropahge Alternative Activation

Project description:Histone Deacetylase 3 is an Epigenomic Brake in Macropahge Alternative Activation

| PRJNA148517 | ENA

Transcriptomic analysis of human polarized macrophages: more than one role of alternative activation?

Project description:Background: Macrophages are a heterogeneous cell population which in response to the cytokine milieu polarize in either classically activated macrophages (M1) or alternatively activated macrophages (M2). This plasticity makes macrophages essential in regulating inflammation, immune response and tissue remodeling and a novel therapeutic target in inflammatory diseases such as atherosclerosis. The aim of the study was to describe the transcriptomic profiles of differently polarized human macrophages to generate new hypotheses on the biological function of the different macrophage subtypes. Methods and Results: M1 polarization was obtained by IFN-γ and LPS, M2a by IL-4, whereas IL-10 induced a “deactivated” state (M2c). Transcription profile of M1, M2a and M2c macrophages was performed at 6, 12 and 24h after polarization with Whole Human Genome Agilent Microarray technique. Gene Ontology (GO) classification revealed that M1 showed a significant up-regulation whereas M2a a down-regulation of GO terms involved in immunity and inflammation compared to resting macrophage (RM). Unexpectedly, canonical and non-canonical Wnt genes and gene groups, promoting inflammation and tissue remodeling, were up-regulated in M2a compared to RM. Key results were confirmed by real time-PCR. Conclusion: Results from gene expression profile confirmed the specific properties of differentially polarized macrophages. However, the enhanced expression of canonical and non-canonical Wnt pathways in M2a suggests a possible dual role for alternative activation in the modulation of low-grade inflammation. Four-condition experiment, RM, M1, M2a, M2c. Three point of time course, three replicates for each condition. Dual color experiment, reference sample: human leucocytes

2015-03-12 | E-GEOD-57614 | biostudies-arrayexpress

Dichotomous Engagement of HDAC3 Activity Governs Inflammatory Responses [RNA-Seq]

Project description:Histone deacetylase 3 (HDAC3) is unique among the HDAC superfamily of chromatin modifiers that silence transcription through enzymatic modification of histones, because interaction with nuclear receptor corepressors (NCoR1/2) is required for engagement of its catalytic activity. However, loss of HDAC3 also represses transcription. Here we report that, during lipopolysaccharide (LPS) activation of macrophages, the deacetylase activity of HDAC3 is selectively engaged at ATF3-bound enhancers that repress anti-inflammatory genes. By contrast, LPS-stimulated recruitment of HDAC3 to ATF2-bound sites without NCoR1/2 activates pro-inflammatory genes by a non-canonical mechanism whereby catalytically inactive HDAC3 stably interacts with p65. Consistent with this bimodal inflammatory modulation, deletion of HDAC3 in macrophages safeguards mice from lethal exposure to LPS, but this protection is not conferred by genetic or pharmacological abolition of HDAC3 catalytic activity. Thus, HDAC3 is a dichotomous transcriptional activator and repressor whose deacetylase-independent functions are critical in priming the innate immune system.

2020-04-30 | GSE140610 | GEO

Dichotomous Engagement of HDAC3 Activity Governs Inflammatory Responses [GRO-Seq]

2020-04-30 | GSE140573 | GEO

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