Requirement for the histone deacetylase Hdac3 for the inflammatory gene expression program in macrophages
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 appr...
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| Published in | Proceedings of the National Academy of Sciences - PNAS Vol. 109; no. 42; pp. 16768 - 16769 |
|---|---|
| Main Authors | , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
National Academy of Sciences
16.10.2012
National Acad Sciences |
| Series | PNAS Plus |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0027-8424 1091-6490 1091-6490 |
| DOI | 10.1073/pnas.1121131109 |
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| Abstract | 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. |
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| AbstractList | 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. 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. Here, we present genetic evidence for the central role of Hdac3 in the inflammatory gene expression program and identify one of the mechanisms involved in this regulation. These data suggest the possible use of selective Hdac3 inhibitors as anti-inflammatory agents. Understanding basic mechanisms of inflammation requires the identification of the sequence-specific transcription factors and transcriptional coregulators that directly control the rapid changes in gene expression that occur on exposure of innate immune response cells, such as macrophages, to inflammatory agents ( 3 ). HDACs deacetylate a large number of substrates, most notably histones, and seem to be required for inflammation as indicated by the known anti-inflammatory activity of pan-HDAC inhibitors, namely, chemicals that nonselectively interfere with the activity of 1 or more of the 11 distinct HDACs. However, the specific family members required for the activation of the inflammatory gene expression program are unknown. In the present study, we used a conditional Hdac3 KO to generate Hdac3-deficient macrophages, in which we characterized both the transcriptional and the genome-wide chromatin changes (histone acetylation) occurring as a consequence of loss of Hdac3 expression. Almost half of LPS-induced genes were down-regulated in KO cells. A major component of the observed defects was the loss of IFN-β production caused by severely impaired Ifnb1 gene activation ( Fig. P1 ). IFN-β controls a large fraction of the secondary gene response (namely, the one requiring new protein synthesis) in this system. Reduced Ifnb1 gene expression is largely ascribed to the overexpression of one of the two rate-limiting enzymes in prostaglandin biosynthesis, Cox-1 ( Fig. P1 ) ( 4 ). Consistent with the inhibitory activity of the molecules produced by Cox-1, including electrophilic oxoderivatives, on Ifnb1 gene expression, blocking the enzymatic activity of Cox-1 with a chemical inhibitor partially rescued the expression of Ifnb1 and its target genes. Cox-1 overexpression correlated with the hyperacetylation of a transcriptional enhancer just upstream of the Ptgs1 gene (encoding Cox-1), which contains several nuclear hormone receptor-binding sites. Because nuclear receptors that are not engaged by their ligands are negatively regulated by Hdac3 -containing complexes with transcriptional repression activity (commonly known as corepressors), these data suggest that Cox-1 overexpression reflects the unopposed activity of nuclear receptors in the absence of Hdac3. Inflammation is a complex response to physical and biological agents, including microbes and endogenous danger signals (e.g., cell debris), and involves the differential expression of hundreds of host genes. The complement of nuclear enzymes (and specifically those controlling covalent histone modifications) that regulates transcription of inflammatory genes has not been fully identified. Histone deacetylases (HDACs) belong to a family of lysine deacetylases targeting histones as well as a large number of nonhistone proteins. Chemical inhibitors of HDACs possess anti-inflammatory activity in various in vitro and in vivo models ( 1 , 2 ), but the specific HDAC(s) involved are unknown. Here, we identify Hdac3 as an essential regulator of the inflammatory transcriptional program. 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. [PUBLICATION ABSTRACT] 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.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. |
| Author | Barozzi, Iros Dalli, Jesmond Recchiuti, Antonio Chen, Xuefen Termanini, Alberto Hiebert, Scott Mietton, Flore Matteoli, Gianluca Prosperini, Elena Natoli, Gioacchino |
| Author_xml | – sequence: 1 givenname: Xuefen surname: Chen fullname: Chen, Xuefen – sequence: 2 givenname: Iros surname: Barozzi fullname: Barozzi, Iros – sequence: 3 givenname: Alberto surname: Termanini fullname: Termanini, Alberto – sequence: 4 givenname: Elena surname: Prosperini fullname: Prosperini, Elena – sequence: 5 givenname: Antonio surname: Recchiuti fullname: Recchiuti, Antonio – sequence: 6 givenname: Jesmond surname: Dalli fullname: Dalli, Jesmond – sequence: 7 givenname: Flore surname: Mietton fullname: Mietton, Flore – sequence: 8 givenname: Gianluca surname: Matteoli fullname: Matteoli, Gianluca – sequence: 9 givenname: Scott surname: Hiebert fullname: Hiebert, Scott – sequence: 10 givenname: Gioacchino surname: Natoli fullname: Natoli, Gioacchino |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/22802645$$D View this record in MEDLINE/PubMed |
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| SubjectTerms | Animals anti-inflammatory activity Anti-inflammatory agents autocrine signaling Base Sequence Binding sites Biological Sciences Chromatin Immunoprecipitation Cyclooxygenase 1 - metabolism Cytokines - analysis DNA Primers - genetics Enzyme-Linked Immunosorbent Assay Flow Cytometry Gene expression gene expression regulation Gene Expression Regulation - genetics genes Genomics histone deacetylase Histone Deacetylases - deficiency Histone Deacetylases - metabolism inflammation interferon-beta macrophages Macrophages - metabolism Membrane Proteins - metabolism Mice Mice, Transgenic Molecular Sequence Data phenotype PNAS Plus PNAS PLUS (AUTHOR SUMMARIES) prostaglandins Proteins Real-Time Polymerase Chain Reaction receptors Reverse Transcriptase Polymerase Chain Reaction Sequence Analysis, DNA T cell receptors |
| Title | Requirement for the histone deacetylase Hdac3 for the inflammatory gene expression program in macrophages |
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