ArticlePain2015
Modality-specific mechanisms of protein kinase C-induced hypersensitivity of TRPV1: S800 is a polymodal sensitization site.
Article in Pain, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.
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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
45 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.
- Targeting TRPV1 channels: new perspectives on the mechanisms of analgesia for herpes zoster neuralgia and advances in therapeutic research.Frontiers in cellular and infection microbiology · 2026Pooled it
- RAGE mediates LPS-induced inflammatory pain in human skin - a double-blind, randomised, placebo-controlled full crossover study.Nature communications · 2026Trial
- Exploring the role of alpha-tocopherol in pain and inflammation: interplay with TRPV1, PKA, and PKC pathways.The Korean journal of pain · 2026Article
- Neuro-immune Crosstalk in Atopic Dermatitis: A Multiaxial Regulatory Network and Novel Therapeutic Perspectives.Clinical reviews in allergy & immunology · 2026Review
- The primary cilium as a compartmentalized signaling hub in tissue immunity and homeostasis.Frontiers in cell and developmental biology · 2026Review
- Brain TRPV1 channel-mediated calcium influx: the immunomodulatory pathway of acupuncture in neuroinflammation.Frontiers in immunology · 2025Review
- Regulatory Action of Calcium and Calcium Channels in Pain Pathways.International journal of biological sciences · 2025Review
- Pinning down a perpetrator in postsurgical eye pain.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- TRPV1 corneal neuralgia mutation: Enhanced pH response, bradykinin sensitization, and capsaicin desensitization.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Oleic acid released by sensory neurons inhibits TRPV1-mediated thermal hypersensitivity via GPR40.iScience · 2024Article
- Exploring oak processionary caterpillar induced lepidopterism (part 2): ex vivo bio-assays unmask the role of TRPV1.Cellular and molecular life sciences : CMLS · 2024Article
- Novel drugs affecting diabetic peripheral neuropathy.Iranian journal of basic medical sciences · 2024Review
- Insulin potentiates the response to capsaicin in dorsal root ganglion neurons in vitro and muscle afferents ex vivo in normal healthy rodents.The Journal of physiology · 2022Article
- An Insight into Potential Pharmacotherapeutic Agents for Painful Diabetic Neuropathy.Journal of diabetes research · 2022Review
- Estrogen-dependent regulation of transient receptor potential vanilloid 1 (TRPV1) and P2X purinoceptor 3 (P2X3): Implication in burning mouth syndrome.Journal of dental sciences · 2022Review
- Bradykinin-Induced Sensitization of Transient Receptor Potential Channel Melastatin 3 Calcium Responses in Mouse Nociceptive Neurons.Frontiers in cellular neuroscience · 2022Article
- TRP Channels as Molecular Targets to Relieve Cancer Pain.Biomolecules · 2021Review
- TRPV1 (Transient Receptor Potential Vanilloid 1) Sensitization of Skeletal Muscle Afferents in Type 2 Diabetic Rats With Hyperglycemia.Hypertension (Dallas, Tex. : 1979) · 2021Article
- The Calcium Signaling Mechanisms in Arterial Smooth Muscle and Endothelial Cells.Comprehensive Physiology · 2021Article
- PKCε stimulation of TRPV1 orchestrates carotid body responses to asthmakines.The Journal of physiology · 2021Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
TRPV1 is a nociceptive ion channel activated by polymodal stimuli such as capsaicin, proton, and noxious heat. Multiple inflammatory mediators activate protein kinases, especially protein kinase C (PKC), which phosphorylates TRPV1. Emerging evidence suggests that phosphorylation of TRPV1 constitutes specific signals underpinning pathological nociception. Although the mechanisms of hypersensitivity of TRPV1 to capsaicin are well studied, the phosphorylation residues that contribute to hypersensitivity to heat or acid have not been identified. In this study, we investigated modality-specific mechanisms of PKC-induced hypersensitivity using mutagenic ablation of PKC-associated phosphorylation sites in TRPV1. In heterologous systems, TRPV1 S502 and S800, but not T704, are known to be involved in hypersensitivity to capsaicin after the application of phorbol myristate acetate (PMA), a PKC agonist. Unlike capsaicin, PMA-induced hypersensitivity to heat was attenuated in TRPV1 mutants T704A and S800A, but not in S502A. In contrast, PMA-induced hypersensitivity to acid was attenuated only in S800A. To examine the roles of these phosphorylation sites in more physiologically relevant conditions, TRPV1 and mutants were tested in sensory neurons from TRPV1-null mice. In sensory neurons expressing mutated TRPV1, we found that alanine mutation of S800 commonly attenuates PMA-induced hypersensitivity to capsaicin, heat, and acid. Moreover, bradykinin-induced hypersensitivity to capsaicin was largely attenuated by the S800A mutation. These results suggest that mechanisms of PKC-induced hypersensitivity of TRPV1 are modality specific and that S800 is a polymodal sensitization site integrating multiple inflammatory signals in nociceptors. Our data provide a rationale for a novel approach targeting TRPV1 S800 for antihyperalgesia.
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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.