ArticleJournal of neuroinflammation2012
Keratinocyte expression of inflammatory mediators plays a crucial role in substance P-induced acute and chronic pain.
Article in Journal of neuroinflammation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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
39 citing papers in PubMed, 64 citations in OpenAlex.
- Comparison of crevicular fluid cytokine levels after the application of surface sealants : A randomized trial.Journal of orofacial orthopedics = Fortschritte der Kieferorthopadie : Organ/official journal Deutsche Gesellschaft fur Kieferorthopadie · 2019Trial
- Inhibition of Janus kinase/signal transducer and activator of transcription reduces nociceptive sensitization in a murine model of complex regional pain syndrome.Pain reports · 2026Article
- Neuro-immune-epithelial pathways involving substance P may contribute to mucosal pathology in gastro-oesophageal reflux disease.Frontiers in immunology · 2026Article
- Article
- Not Just Neurons: Pain Is Orchestrated in Partnership with Many Non-neuronal Cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Review
- Light repair effect of polysaccharides component from white Ganoderma lucidum and Laminaria japonica fermentation broth attenuates epidermal barrier dysfunction via TRPV4-Keap-1/Nrf2 pathway.Bioresources and bioprocessing · 2025Article
- Alpha-7 Nicotinic Acetylcholine Receptor Activation Inhibits Trauma Induced Pronociceptive Autoimmune Responses.The journal of pain · 2024Article
- Nerve Growth Factor Shows Biphasic Expression during Adjuvant-Induced Neurogenic Inflammation.International journal of molecular sciences · 2024Article
- Harnessing strategies for enhancing diabetic wound healing from the perspective of spatial inflammation patterns.Bioactive materials · 2023Review
- Neuropathic pain; what we know and what we should do about it.Frontiers in pain research (Lausanne, Switzerland) · 2023Review
- Emerging roles of keratinocytes in nociceptive transduction and regulation.Frontiers in molecular neuroscience · 2022Review
- An Unusual Case of Periosteal Glomus Tumor at the Metacarpal Base Presenting as Type II CRPS: Case Report.Hand (New York, N.Y.) · 2021Article
- Article
- Article
- Substance P as a potential biomarker of pain assessment in dogs.Iranian journal of veterinary research · 2019Article
- The Rodent Tibia Fracture Model: A Critical Review and Comparison With the Complex Regional Pain Syndrome Literature.The journal of pain · 2018Review
- Oxidative Stress Contributes to Fracture/Cast-Induced Inflammation and Pain in a Rat Model of Complex Regional Pain Syndrome.The journal of pain · 2018Article
- Exercise Reverses Nociceptive Sensitization, Upregulated Neuropeptide Signaling, Inflammatory Changes, Anxiety, and Memory Impairment in a Mouse Tibia Fracture Model.Anesthesiology · 2018Article
- Neuropeptide regulation of adaptive immunity in the tibia fracture model of complex regional pain syndrome.Journal of neuroinflammation · 2018Article
- Negative Pressure Therapy in the Regeneration of the Sciatic Nerve Using Vacuum - Assisted Closure in a Rabbit Model.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Tibia fracture in rats followed by cast immobilization leads to nociceptive, trophic, vascular and bone-related changes similar to those seen in Complex Regional Pain Syndrome (CRPS). Substance P (SP) mediated neurogenic inflammation may be responsible for some of the signs of CRPS in humans. We therefore hypothesized that SP acting through the SP receptor (NK1) leads to the CRPS-like changes found in the rat model. In the present study, we intradermally injected rats with SP and monitored hindpaw mechanical allodynia, temperature, and thickness as well as tissue levels of tumor necrosis factor-α (TNF-α), interleukin 1β (IL-1β), interleukin 6 (IL-6), and nerve growth factor-β (NGF) for 72 h. Anti-NGF antibody was utilized to block the effects of SP-induced NGF up-regulation. Fracture rats treated with the selective NK1 receptor antagonist LY303870 prior to cast removal were assessed for BrdU, a DNA synthesis marker, incorporation in skin cells to examine cellular proliferation. Bone microarchitecture was measured using micro computed tomography (μCT). We observed that: (1) SP intraplantar injection induced mechanical allodynia, warmth and edema as well as the expression of nociceptive mediators in the hindpaw skin of normal rats, (2) LY303870 administered intraperitoneally after fracture attenuated allodynia, hindpaw unweighting, warmth, and edema, as well as cytokine and NGF expression, (3) LY303870 blocked fracture-induced epidermal thickening and BrdU incorporation after fracture, (4) anti-NGF antibody blocked SP-induced allodynia but not warmth or edema, and (5) LY303870 had no effect on bone microarchitecture. Collectively our data indicate that SP acting through NK1 receptors supports the nociceptive and vascular components of CRPS, but not the bone-related changes.
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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.