ArticleImmunology and cell biology2019
Histone deacetylase 2 is essential for LPS-induced inflammatory responses in macrophages.
Article in Immunology and cell biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.
- Epigenetic mechanisms of Immune remodeling in sepsis: targeting histone modification.Cell death & disease · 2023Pooled it
- HDAC2 enhances the antimicrobial activity of neutrophils by promoting the formation of neutrophil extracellular traps (NETs) in sepsis.Journal of advanced research · 2026Article
- Epigenetic Regulation of Inflammation by Dopamine in Primary Human Macrophages.bioRxiv : the preprint server for biology · 2026Article
- Epigenetic regulation of inflammation by dopamine in primary human macrophages.Frontiers in immunology · 2026Article
- HDAC4 Promotes Neuroprotection of Retinal Ganglion Cells After Optic Nerve Injury.Investigative ophthalmology & visual science · 2025Article
- Protein acylation in inflammatory diseases: from mechanisms to therapeutic strategies.Cell communication and signaling : CCS · 2025Review
- Unravelling butyrate metabolism in sepsis: identification of key genes.BMC infectious diseases · 2025Article
- Cigarette smoking induces NLRP3 inflammasome activation in patients with atrial fibrillation.American journal of physiology. Heart and circulatory physiology · 2025Article
- HDAC2 mediates the activation of macrophage in sepsis induced lung injury via regulating the acetylation of SOX2 and the transcription of STAMP2.European journal of medical research · 2025Article
- Molecular mechanisms and functions of protein acetylation in sepsis and sepsis-associated organ dysfunction.Cellular & molecular biology letters · 2025Review
- Mechanisms of Impaired Wound Healing in Type 2 Diabetes: The Role of Epigenetic Factors.Arteriosclerosis, thrombosis, and vascular biology · 2025Review
- Regulation of Histone Acetylation During Inflammation Resolution.ImmunoTargets and therapy · 2025Article
- Metabolic Endotoxemia: From the Gut to Neurodegeneration.International journal of molecular sciences · 2024Review
- Microglial histone deacetylase 2 is dispensable for functional and histological outcomes in a mouse model of traumatic brain injury.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024Article
- The monocyte-derived cytokine response in whole blood from preterm newborns against sepsis-related bacteria is similar to term newborns and adults.Frontiers in immunology · 2024Article
- ROS signaling in innate immunity via oxidative protein modifications.Frontiers in immunology · 2024Review
- Suppressed oncogenic molecules involved in the treatment of colorectal cancer by fecal microbiota transplantation.Frontiers in microbiology · 2024Article
- The Role of Histone Deacetylases in Acute Lung Injury-Friend or Foe.International journal of molecular sciences · 2023Review
- Article
- Porcine Deltacoronavirus Infection Cleaves HDAC2 to Attenuate Its Antiviral Activity.Journal of virology · 2022Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The role of specific histone deacetylase (HDAC) proteins in regulating the lipopolysaccharide (LPS)-induced inflammatory response and its underlying mechanisms are unclear. Here, HDAC2, a class I HDAC family protein, is essential for the LPS-triggered inflammatory response in macrophages. LPS stimulation increases HDAC2 expression in macrophages. Knockdown of HDAC2 decreases the expression of proinflammatory genes, such as IL-12, TNF-α and iNOS following stimulation with LPS. The adoptive transfer of HDAC2 knockdown macrophages attenuates the LPS-triggered innate inflammatory response in vivo, and these mice are less sensitive to endotoxin shock and Escherichia coli-induced sepsis. Mechanistically, the c-Jun protein is the main target of HDAC2-mediated LPS-induced production of proinflammatory cytokines. Moreover, HDAC2 knockdown increases the expression of c-Jun, which directly binds the promoters of proinflammatory genes and forms nuclear receptor corepressor complexes to inhibit the transcription of proinflammatory genes in macrophages. These effects are rescued by c-Jun expression. According to the chromatin immunoprecipitation analysis, HDAC2 also selectively suppresses c-Jun expression by directly binding to its promoter and modifying histone acetylation after LPS stimulation. Our findings define a new function and mechanism of the HDAC2/c-Jun signaling network that regulates the LPS-induced immune response in macrophages.
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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.