ArticleScientific reports2017
RNA sequencing reveals resistance of TLR4 ligand-activated microglial cells to inflammation mediated by the selective jumonji H3K27 demethylase inhibitor.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 33 citations in OpenAlex.
- Microglia activation by derepression of endogenous retroviruses drives inflammation and cellular senescence.Nature neuroscience · 2026Article
- Epigenetic regulation of TIMP-3 expression in human macrophages via physiological and pharmacological modification of histone3 lysine27 (H3K27).Molecular biology reports · 2025Article
- 18 kDa TSPO targeting drives polarized human microglia towards a protective and restorative neurosteroidome profile.Cellular and molecular life sciences : CMLS · 2025Article
- Neonatal immune challenge poses a sex-specific risk for epigenetic microglial reprogramming and behavioral impairment.Nature communications · 2023Article
- Lumateperone Normalizes Pathological Levels of Acute Inflammation through Important Pathways Known to Be Involved in Mood Regulation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Epigenetics and immune cells in medulloblastoma.Frontiers in genetics · 2023Review
- Hypoxia induced-disruption of lncRNA TUG1/PRC2 interaction impairs human trophoblast invasion through epigenetically activating Nodal/ALK7 signalling.Journal of cellular and molecular medicine · 2022Article
- Systematic identification of biomarker-driven drug combinations to overcome resistance.Nature chemical biology · 2022Article
- Microglial Polarization: Novel Therapeutic Strategy against Ischemic Stroke.Aging and disease · 2021Review
- Epigenetic Control of Autophagy Related Genes Transcription in Pulpitis via JMJD3.Frontiers in cell and developmental biology · 2021Article
- Article
- JMJD3 in the regulation of human diseases.Protein & cell · 2019Review
- DHEA Attenuates Microglial Activation via Induction of JMJD3 in Experimental Subarachnoid Haemorrhage.Journal of neuroinflammation · 2019Article
- Article
- Small Molecule GSK-J1 Affects Differentiation of Specific Neuronal Subtypes in Developing Rat Retina.Molecular neurobiology · 2019Article
- Histone demethylase UTX is a therapeutic target for diabetic kidney disease.The Journal of physiology · 2019Article
- RNA-Seq transcriptomic profiling of primary murine microglia treated with LPS or LPS + IFNγ.Scientific reports · 2018Article
- Electric Stimulation of Ear Reduces the Effect of Toll-Like Receptor 4 Signaling Pathway on Kainic Acid-Induced Epileptic Seizures in Rats.BioMed research international · 2018Article
- Butyrate and Dietary Soluble Fiber Improve Neuroinflammation Associated With Aging in Mice.Frontiers in immunology · 2018Article
- Epigenetics Control Microglia Plasticity.Frontiers in cellular neuroscience · 2018Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Persistent microglial activation is associated with the production and secretion of various pro-inflammatory genes, cytokines and chemokines, which may initiate or amplify neurodegenerative diseases. A novel synthetic histone 3 lysine 27 (H3K27) demethylase JMJD3 inhibitor, GSK-J4, was proven to exert immunosuppressive activities in macrophages. However, a genome-wide search for GSK-J4 molecular targets has not been undertaken in microglia. To study the immuno-modulatory effects of GSK-J4 at the transcriptomic level, triplicate RNA sequencing and quantitative real-time PCR analyses were performed with resting, GSK-J4-, LPS- and LPS + GSK-J4-challenged primary microglial (PM) and BV-2 microglial cells. Among the annotated genes, the transcriptional sequencing of microglia that were treated with GSK-J4 revealed a selective effect on LPS-induced gene expression, in which the induction of cytokines/chemokines, interferon-stimulated genes, and prominent transcription factors TFs, as well as previously unidentified genes that are important in inflammation was suppressed. Furthermore, we showed that GSK-J4 controls are important inflammatory gene targets by modulating STAT1, IRF7, and H3K27me3 levels at their promoter sites. These unprecedented results demonstrate that the histone demethylase inhibitor GSK-J4 could have therapeutic applications for neuroinflammatory diseases.
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