ArticleJournal of neuroinflammation2020
TDAG8 deficiency reduces satellite glial number and pro-inflammatory macrophage number to relieve rheumatoid arthritis disease severity and chronic pain.
Article in Journal of neuroinflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 31 citations in OpenAlex.
- Loss of proton-sensing TDAG8 increases tumor progression in mouse models of colon cancer.Molecular oncology · 2026Article
- Effects of methotrexate on Wnt/β-catenin signaling and glial activation in temporomandibular joint arthritis in rats.European journal of oral sciences · 2025Article
- GPR65 Functions as a Key Factor of Bone Aging and a Novel Therapeutic Target for Osteoporosis.Aging cell · 2025Article
- Activation of the proton-sensing GPCR, GPR65 on fibroblast-like synoviocytes contributes to inflammatory joint pain.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Single-cell RNA sequencing reveals the CRTAC1Aging cell · 2024Article
- T cell death-associated gene 8-mediated distinct signaling pathways modulate the early and late phases of neuropathic pain.iScience · 2024Article
- Review
- Immunomodulation of Proton-activated G Protein-coupled Receptors in Inflammation.Current medical science · 2024Review
- Recent advances in acid sensing by G protein coupled receptors.Pflugers Archiv : European journal of physiology · 2024Review
- Article
- The Novel Small Molecule BTB Inhibits Pro-Fibrotic Fibroblast Behavior though Inhibition of RhoA Activity.International journal of molecular sciences · 2022Article
- Osteoporosis in patients with rheumatoid arthritis is associated with serum immune regulatory cellular factors.Clinical rheumatology · 2022Article
- Gut Mucosal Microbiome Is Perturbed in Rheumatoid Arthritis Mice and Partly Restored after TDAG8 Deficiency or Suppression by Salicylanilide Derivative.International journal of molecular sciences · 2022Article
- Sinomenine regulates immune cell subsets: Potential neuro-immune intervene for precise treatment of chronic pain.Frontiers in cell and developmental biology · 2022Review
- Macrophages and glial cells: Innate immune drivers of inflammatory arthritic pain perception from peripheral joints to the central nervous system.Frontiers in pain research (Lausanne, Switzerland) · 2022Review
- Identification and Validation of Prognostic Biomarkers Specifically Expressed in Macrophage in IgA Nephropathy Patients Based on Integrated Bioinformatics Analyses.Frontiers in molecular biosciences · 2022Article
- LCC-09, a Novel Salicylanilide Derivative, Exerts Anti-Inflammatory Effect in Vascular Endothelial Cells.Journal of inflammation research · 2021Article
- Article
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundThe autoimmune disease rheumatoid arthritis (RA) affects approximately 1% of the global population. RA is characterized with chronic joint inflammation and often associated with chronic pain. The imbalance of pro-inflammatory and anti-inflammatory macrophages is a feature of RA progression. Glial cells affecting neuronal sensitivity at both peripheral and central levels may also be important for RA progression and associated pain. Genetic variants in the T cell death-associated gene 8 (TDAG8) locus are found to associate with spondyloarthritis. TDAG8 was also found involved in RA disease progression and associated hyperalgesia in the RA mouse model. However, its modulation in RA remains unclear.
methodsTo address this question, we intra-articularly injected complete Freund's adjuvant (CFA) into TDAG8
resultsWe demonstrated that TDAG8 deletion slightly reduced RA pain in the early phase but dramatically attenuated RA progression and pain in the chronic phase (> 7 weeks). TDAG8 deletion inhibited an increase in SGC number and inhibition of SGC function attenuated chronic phase of RA pain, so TDAG8 could regulate SGC number to control chronic pain. TDAG8 deletion also reduced M1 pro-inflammatory macrophage number at 12 weeks, contributing to the attenuation of chronic RA pain. Such results were further confirmed by using salicylanilide derivatives, CCL-2d or LCC-09, to suppress TDAG8 expression and function.
conclusionsThis study demonstrates that TDAG8 deletion reduced SGC and M1 macrophage number to relieve RA disease severity and associated chronic pain. M1 macrophages are critical for the development and maintenance of RA disease and pain, but glial activation is also required for the chronic phase of RA pain.
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Registered trials
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