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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE33596 | GEO | 2011/11/10

SECONDARY ACCESSION(S): PRJNA154331

REPOSITORIES: GEO

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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 (microarray)

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Nuclear Receptor Corepressors are Required for the Histone Deacetylase Activity of HDAC3 In Vivo (ChIP-Seq)

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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

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Project description:Macrophages, a key cellular component of inflammation, become functionally polarized in a signal- and context-specific manner. Th2 cytokines such as interleukin 4 (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. Here we report that macrophages lacking histone deacetylase 3 (HDAC3) display a polarization phenotype similar to IL-4-induced alternative activation and, furthermore, are hyperresponsive to IL-4 stimulation. Throughout the macrophage genome, HDAC3 deacetylates histone tails at regulatory regions, leading to repression of many IL-4-regulated genes characteristic of alternative activation. Following exposure to Schistosoma mansoni eggs, a model of Th2 cytokine-mediated disease that is limited by alternative activation, pulmonary inflammation was ameliorated in mice lacking HDAC3 in macrophages. Thus, HDAC3 functions in alternative activation as a brake whose release could be of benefit in the treatment of multiple inflammatory diseases.

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