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Histone Deacetylase 3 is an Epigenomic Brake in Macropahge Alternative Activation

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

PROVIDER: PRJNA148517 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR363749.fastq.gz	Fastqsanger.gz
	SRR363750.fastq.gz	Fastqsanger.gz
	SRR363751.fastq.gz	Fastqsanger.gz
	SRR363752.fastq.gz	Fastqsanger.gz
	SRR363753.fastq.gz	Fastqsanger.gz

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Similar Datasets

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

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 (microarray)

2011-11-10 | GSE33608 | GEO

Histone deacetylase 3 is an epigenomic brake in macrophage alternative activation.

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.

| S-EPMC3243058 | biostudies-literature

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 SubSeries listed below.

2011-11-10 | GSE33609 | GEO

Mus musculus

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

| PRJNA154329 | ENA

Mus musculus

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

| PRJNA154331 | ENA

Histone deacetylase activity modulates alternative splicing.

Project description:There is increasing evidence to suggest that splicing decisions are largely made when the nascent RNA is still associated with chromatin. Here we demonstrate that activity of histone deacetylases (HDACs) influences splice site selection. Using splicing-sensitive microarrays, we identified ∼700 genes whose splicing was altered after HDAC inhibition. We provided evidence that HDAC inhibition induced histone H4 acetylation and increased RNA Polymerase II (Pol II) processivity along an alternatively spliced element. In addition, HDAC inhibition reduced co-transcriptional association of the splicing regulator SRp40 with the target fibronectin exon. We further showed that the depletion of HDAC1 had similar effect on fibronectin alternative splicing as global HDAC inhibition. Importantly, this effect was reversed upon expression of mouse HDAC1 but not a catalytically inactive mutant. These results provide a molecular insight into a complex modulation of splicing by HDACs and chromatin modifications.

| S-EPMC3032741 | biostudies-literature

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