ArticleInternational journal of oral science2019
Activation of mitogen-activated protein kinases in satellite glial cells of the trigeminal ganglion contributes to substance P-mediated inflammatory pain.
Article in International journal of oral science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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25 citing papers in PubMed, 47 citations in OpenAlex.
- Substance P induces sympathetic immune response in the contralateral eye after the first eye cataract surgery in type 2 diabetic patients.BMC ophthalmology · 2020Trial
- Peripheral Nerve Injury Induces an Interferon-Responsive State Centered on Satellite Glial Cells in the DRG That Sustains Neuropathic Pain Through STAT1 and CXCL10 Signaling.Brain sciences · 2026Article
- A dual role of PIEZO2 in neuropathic pain: driving peripheral sensitization and enabling mechanical loading-induced analgesia.Cell communication and signaling : CCS · 2026Article
- Muscle-Nerve Signaling and Neurogenic Inflammation in Temporomandibular Disorders: Potential Contributions of Occlusal Interference and Other Peripheral Triggers.Dentistry journal · 2026Review
- Triple Latency as a Driver of Chronic Inflammation: An Integrative View of HSV, EBV, and CMV Persistence in Immunocompetent Hosts.Clinics and practice · 2026Review
- Neuroregulatory Biomaterials for Intervertebral Disc Regeneration via Neuro-Disc Microenvironment Modulation.Research (Washington, D.C.) · 2026Review
- (-)-Epicatechin and inflammation: Unraveling the role of microbial metabolites and interindividual metabolic variability.Frontiers in microbiology · 2026Review
- Trigeminal nerve root compression induced neuroinflammatory response promotes mechanical allodynia through the CGRP/SP-Piezo2 axis via CaCellular & molecular biology letters · 2025Article
- Unraveling the neuroimmune mechanisms in cancer-induced bone pain: New horizons for therapeutic intervention of the two-phase paradigm.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Temporomandibular disorders and mental health: shared etiologies and treatment approaches.The journal of headache and pain · 2025Review
- HDAC inhibitors as a potential therapy for chemotherapy-induced neuropathic pain.Inflammopharmacology · 2024Review
- Identification of Oxidative Stress-Related Biomarkers for Pain-Depression Comorbidity Based on Bioinformatics.International journal of molecular sciences · 2024Article
- Pathology of pain and its implications for therapeutic interventions.Signal transduction and targeted therapy · 2024Review
- Changes in serum levels of pain mediators in hemiplegic shoulder pain.Brain and behavior · 2023Article
- Article
- Role of inflammation and oxidative stress in chemotherapy-induced neurotoxicity.Immunologic research · 2022Review
- Identification of Novel Genetic Variants Associated with Insomnia and Migraine Comorbidity.Nature and science of sleep · 2022Article
- PKCζ-Mitogen-Activated Protein Kinase Signaling Mediates Crotalphine-Induced Antinociception.Toxins · 2021Article
- NFAT5 Deficiency Alleviates Formalin-Induced Inflammatory Pain Through mTOR.International journal of molecular sciences · 2021Article
- Novel Analgesics with Peripheral Targets.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2020Review
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammatory orofacial pain, in which substance P (SP) plays an important role, is closely related to the cross-talk between trigeminal ganglion (TG) neurons and satellite glial cells (SGCs). SGC activation is emerging as the key mechanism underlying inflammatory pain through different signalling mechanisms, including glial fibrillary acidic protein (GFAP) activation, phosphorylation of mitogen-activated protein kinase (MAPK) signalling pathways, and cytokine upregulation. However, in the TG, the mechanism underlying SP-mediated orofacial pain generated by SGCs is largely unknown. In this study, we investigated whether SP is involved in inflammatory orofacial pain by upregulating interleukin (IL)-1β and tumour necrosis factor (TNF)-α from SGCs, and we explored whether MAPK signalling pathways mediate the pain process. In the present study, complete Freund's adjuvant (CFA) was injected into the whisker pad of rats to induce an inflammatory model in vivo. SP was administered to SGC cultures in vitro to confirm the effect of SP. Facial expression analysis showed that pre-injection of L703,606 (an NK-1 receptor antagonist), U0126 (an inhibitor of MAPK/extracellular signal-regulated kinase [ERK] kinase [MEK] 1/2), and SB203580 (an inhibitor of P38) into the TG to induce targeted prevention of the activation of the NK-1 receptor and the phosphorylation of MAPKs significantly suppressed CFA-induced inflammatory allodynia. In addition, SP promoted SGC activation, which was proven by increased GFAP, p-MAPKs, IL-1β and TNF-α in SGCs under inflammatory conditions. Moreover, the increase in IL-1β and TNF-α was suppressed by L703, 606, U0126 and SB203580 in vivo and in vitro. These present findings suggested that SP, released from TG neurons, activated SGCs through the ERK1/2 and P38 pathways and promoted the production of IL-1β and TNF-α from SGCs, contributing to inflammatory orofacial pain associated with peripheral sensitization.
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