ArticleCellular signalling2014
Jmjd3-mediated epigenetic regulation of inflammatory cytokine gene expression in serum amyloid A-stimulated macrophages.
Article in Cellular signalling, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
50 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 citations in OpenAlex.
- Targeting epigenetics and non-coding RNAs in atherosclerosis: from mechanisms to therapeutics.Pharmacology & therapeutics · 2019Pooled it
- Trial
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- Regulation of histone H3K27 methylation in inflammation and cancer.Molecular biomedicine · 2025Review
- Emerging role of Jumonji domain-containing protein D3 in inflammatory diseases.Journal of pharmaceutical analysis · 2024Review
- Histone demethylases in the regulation of immunity and inflammation.Cell death discovery · 2023Review
- The H3K27 demethylase controls the lateral line embryogenesis of zebrafish.Cell biology and toxicology · 2023Article
- Role of Jumonji domain-containing protein D3 and its inhibitor GSK-J4 in Hashimoto's thyroiditis.Open medicine (Warsaw, Poland) · 2023Article
- Innate Immune Memory in Monocytes and Macrophages: The Potential Therapeutic Strategies for Atherosclerosis.Cells · 2022Review
- Downregulation of interleukin-1 beta via Jmjd3 inhibition improves post-myocardial infarction depression.Cardiovascular diagnosis and therapy · 2022Article
- The Epigenome in Atherosclerosis.Handbook of experimental pharmacology · 2022Article
- The JMJD Family Histone Demethylases in Crosstalk Between Inflammation and Cancer.Frontiers in immunology · 2022Review
- Diverse Epigenetic Regulations of Macrophages in Atherosclerosis.Frontiers in cardiovascular medicine · 2022Review
- Human umbilical cord mesenchymal stem cells ameliorate depression by regulating Jmjd3 and microglia polarization in myocardial infarction mice.Psychopharmacology · 2021Article
- Targeting epigenetic modifiers to reprogramme macrophages in non-resolving inflammation-driven atherosclerosis.European heart journal open · 2021Article
- SAA1 regulates pro-labour mediators in term labour by activating YAP pathway.Molecular and cellular biochemistry · 2021Article
- Inhibition of macrophage histone demethylase JMJD3 protects against abdominal aortic aneurysms.The Journal of experimental medicine · 2021Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Serum amyloid A (SAA), a major acute-phase protein, has potent cytokine-like activities in isolated phagocytes and synovial fibroblasts. SAA-induced proinflammatory cytokine gene expression requires transcription factors such as NF-κB; however, the associated epigenetic regulatory mechanism remains unclear. Here we report that Jmjd3, a histone H3 lysine 27 (H3K27) demethylase, is highly inducible in SAA-stimulated macrophages and plays an important role in the induction of inflammatory cytokine genes. SAA-induced Jmjd3 expression leads to reduced H3K27 trimethylation. Silencing of Jmjd3 expression significantly inhibited SAA-induced expression of proinflammatory cytokines including IL-23p19, G-CSF and TREM-1, along with up-regulation of H3K27 trimethylation levels on their promoters. Depletion of Jmjd3 expression also attenuated the release of proinflammatory cytokine genes in a peritonitis model and ameliorated neutrophilia in SAA-stimulated mice. Finally, we observed that Jmjd3 is essential for SAA-enhanced macrophage foam cell formation by oxidized LDL. Taken together, these results illustrate a Jmjd3-dependent epigenetic regulatory mechanism for proinflammatory cytokine gene expression in SAA-stimulate macrophages. This mechanism may be subject to therapeutic intervention for sterile inflammation and atherosclerosis.
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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.