ArticleThe Journal of biological chemistry2012
Histone deacetylase 3 mediates allergic skin inflammation by regulating expression of MCP1 protein.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 63 citations in OpenAlex.
- Mast cell-derived extracellular vesicles in lung diseases: roles in pulmonary inflammation, immune regulation, and microenvironmental remodeling.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Serum HDAC3 as an early biomarker for prediction and staging of sepsis-associated AKI: prospective cohort study.BMC infectious diseases · 2026Article
- The role of protein lactylation in skin diseases: from molecular mechanisms to potential therapeutics.Frontiers in immunology · 2026Review
- Transcriptional Repression of CCL2 by KInternational journal of molecular sciences · 2025Article
- Histone Deacetylases (HDACs) Roles in Inflammation-mediated Diseases; Current Knowledge.Cell biochemistry and biophysics · 2025Review
- The role of HDAC3 in inflammation: mechanisms and therapeutic implications.Frontiers in immunology · 2024Review
- An antioxidant ameliorates allergic airway inflammation by inhibiting HDAC 1 via HIF-1α/VEGF axis suppression in mice.Scientific reports · 2023Article
- Machine learning-based identification of CYBB and FCAR as potential neutrophil extracellular trap-related treatment targets in sepsis.Frontiers in immunology · 2023Article
- The Crosstalk between FcεRI and Sphingosine Signaling in Allergic Inflammation.International journal of molecular sciences · 2022Review
- Critical Functions of Histone Deacetylases (HDACs) in Modulating Inflammation Associated with Cardiovascular Diseases.Pathophysiology : the official journal of the International Society for Pathophysiology · 2022Review
- Post-Translational Modifications in Atopic Dermatitis: Current Research and Clinical Relevance.Frontiers in cell and developmental biology · 2022Review
- HDAC inhibitor, MS-275, increases vascular permeability by suppressing Robo4 expression in endothelial cells.Tissue barriers · 2021Article
- Effect of commonly used cosmetic preservatives on skin resident microflora dynamics.Scientific reports · 2021Article
- High-Throughput Screening for CEBPD-Modulating Compounds in THP-1-Derived Reporter Macrophages Identifies Anti-Inflammatory HDAC and BET Inhibitors.International journal of molecular sciences · 2021Article
- MiR-154-5p-MCP1 Axis Regulates Allergic Inflammation by Mediating Cellular Interactions.Frontiers in immunology · 2021Article
- EGR3-HDAC6-IL-27 Axis Mediates Allergic Inflammation and Is Necessary for Tumorigenic Potential of Cancer Cells Enhanced by Allergic Inflammation-Promoted Cellular Interactions.Frontiers in immunology · 2021Article
- Chemokines during anaphylaxis: the importance of CCL2 and CCL2-dependent chemotactic activity for basophils.Clinical and translational allergy · 2020Article
- Homoharringtonine Inhibits Allergic Inflammations by Regulating NF-κB-miR-183-5p-BTG1 Axis.Frontiers in pharmacology · 2020Article
- Synergistic Enhancement of Cancer Therapy Using HDAC Inhibitors: Opportunity for Clinical Trials.Frontiers in genetics · 2020Review
- FcεRI-HDAC3-MCP1 Signaling Axis Promotes Passive Anaphylaxis Mediated by Cellular Interactions.International journal of molecular sciences · 2019Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have shown the induction of histone deacetylase 3 (HDAC3) in antigen-stimulated rat basophilic leukemia cells via NF-κB. We investigated the role of HDAC3 in allergic skin inflammation. We used a BALB/c mouse model of triphasic cutaneous anaphylaxis (triphasic cutaneous reaction; TpCR) and passive cutaneous anaphylaxis (PCA) to examine the role of HDAC3 in allergic skin inflammation. Triphasic cutaneous reaction involved induction of HDAC3 and was mediated by HDAC3. HDAC3 showed an interaction with FcεRIβ. Trichostatin A (TSA), an inhibitor of HDAC(s), disrupted this interaction. Cytokine array analysis showed that the down-regulation of HDAC3 led to the decreased secretion of monocyte chemoattractant protein 1 (MCP1). FcεRI was necessary for induction of HDAC3 and MCP1. ChIP assays showed that HDAC3, in association with Sp1 and c-Jun, was responsible for induction of MCP1 expression. TSA exerted a negative effect on induction of MCP1. HDAC3 exerted a negative regulation on expression of HDAC2 via interaction with Rac1. The down-regulation of HDAC3 or inactivation of Rac1 induced binding of HDAC2 to MCP1 promoter sequences. TSA exerted a negative effect on HDAC3-mediated TpCR. The BALB/c mouse model of PCA involved induction of HDAC3 and MCP1. HDAC3 and MCP1 were necessary for PCA that involved ear swelling, enhanced vascular permeability, and angiogenesis. Recombinant MCP1 enhanced β-hexosaminidase activity and histamine release and also showed angiogenic potential. TSA exerted a negative effect on PCA. Our data show HDAC3 as a valuable target for the development of allergic skin inflammation therapeutics.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.