ArticleScientific reports2017
TDAG8 involved in initiating inflammatory hyperalgesia and establishing hyperalgesic priming in mice.
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 17 papers.
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- Inhibition of GPR4 Ameliorates Neuropathic Pain and Neuronal Ferroptosis via Regulation of Spinal RhoA/YAP Signaling in Rats.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026Article
- 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
- T cell death-associated gene 8-mediated distinct signaling pathways modulate the early and late phases of neuropathic pain.iScience · 2024Article
- The role of orphan G protein-coupled receptors in pain.Heliyon · 2024Review
- MicroRNAs combined with the TLR4/TDAG8 mRNAs and proinflammatory cytokines are biomarkers for the rapid diagnosis of sepsis.Molecular medicine reports · 2022Article
- IBD-associated G protein-coupled receptor 65 variant compromises signalling and impairs key functions involved in inflammation.Cellular signalling · 2022Article
- Proton-Sensing GPCRs in Health and Disease.Cells · 2021Review
- Electroacupuncture Regulates Pain Transition Through Inhibiting PKCε and TRPV1 Expression in Dorsal Root Ganglion.Frontiers in neuroscience · 2021Article
- Proton Sensing on the Ocular Surface: Implications in Eye Pain.Frontiers in pharmacology · 2021Review
- TDAG8 deficiency reduces satellite glial number and pro-inflammatory macrophage number to relieve rheumatoid arthritis disease severity and chronic pain.Journal of neuroinflammation · 2020Article
- Temporal expression patterns of distinct cytokines and M1/M2 macrophage polarization regulate rheumatoid arthritis progression.Molecular biology reports · 2020Article
- Acupuncture alleviates acid- and purine-induced pain in rodents.British journal of pharmacology · 2020Article
- Evolution of acid nociception: ion channels and receptors for detecting acid.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2019Review
- Mu-opioid Receptor (MOR) Biased Agonists Induce Biphasic Dose-dependent Hyperalgesia and Analgesia, and Hyperalgesic Priming in the Rat.Neuroscience · 2018Article
- G2A as a Threshold Regulator of Inflammatory Hyperalgesia Modulates Chronic Hyperalgesia.Journal of molecular neuroscience : MN · 2018Article
- Involvement of Opioid System, TRPM8, and ASIC Receptors in Antinociceptive Effect of Arrabidaea brachypoda (DC) Bureau.International journal of molecular sciences · 2017Article
- TDAG8, TRPV1, and ASIC3 involved in establishing hyperalgesic priming in experimental rheumatoid arthritis.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic pain, resulting from injury, arthritis, and cancer, is often accompanied by inflammation. High concentrations of protons found in inflamed tissues results in tissue acidosis, a major cause of pain and hyperalgesia. Acidosis signals may mediate a transition from acute to chronic hyperalgesia (hyperalgesic priming) via proton-sensing G-protein-coupled receptors (GPCRs). The expression of T-cell death-associated gene 8 (TDAG8), a proton-sensing GPCR, is increased during inflammatory hyperalgesia. Attenuating TDAG8 expression in the spinal cord inhibits bone cancer pain, but whether TDAG8 is involved in inflammatory hyperalgesia or hyperalgesic priming remains unclear. In this study, we used TDAG8-knockout or -knockdown to explore the role of TDAG8 in pain. Suppressed TDAG8 expression delayed the onset of inflammatory hyperalgesia and shortened hyperalgesic time in mice. In a dual acid-injection model (acid [pH 5.0] injected twice, 5 days apart), shRNA inhibition of TDAG8 shortened the duration of the second hyperalgesia. Similar results were found in TDAG8-deficient mice. The dual administration of TDAG8 agonist also confirmed that TDAG8 is involved in hyperalgsic priming. Accordingly, TDAG8 may mediate acidosis signals to initiate inflammatory hyperalgesia and establish hyperalgesic priming.
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