ArticleNeuroscience bulletin2016
Modulation of Nav1.8 by Lysophosphatidic Acid in the Induction of Bone Cancer Pain.
Article in Neuroscience bulletin, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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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.
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Who cites it
23 citing papers in PubMed, 32 citations in OpenAlex.
- LPA/LPAR signaling drives temporomandibular disorders-like pain through regulating the expression and sensitization of PIEZO2.Science advances · 2026Article
- Central Sensitization and Nociplastic Pain: Shared Mechanisms in Fibromyalgia, Osteoarthritis, and Inflammatory Arthritis.Journal of pain research · 2026Review
- Long noncoding RNA NONRATT007487.2 drives cancer-induced bone pain progression through direct interaction with CXCL1.The Korean journal of pain · 2025Article
- Unveiling the therapeutic promise: exploring Lysophosphatidic Acid (LPA) signaling in malignant bone tumors for novel cancer treatments.Lipids in health and disease · 2024Review
- Peripheral Mechanism of Cancer-Induced Bone Pain.Neuroscience bulletin · 2024Review
- A novel co-target of ACY1 governing plasma membrane translocation of SphK1 contributes to inflammatory and neuropathic pain.iScience · 2023Article
- Analgesic effect of electroacupuncture on bone cancer pain in rat model: the role of peripheral P2X3 receptor.Purinergic signalling · 2023Article
- Targeting autotaxin impacts disease advance in the SOD1-G93A mouse model of amyotrophic lateral sclerosis.Brain pathology (Zurich, Switzerland) · 2022Article
- Enhancement of P2X3 Receptor-Mediated Currents by Lysophosphatidic Acid in Rat Primary Sensory Neurons.Frontiers in pharmacology · 2022Article
- The Roles of Lpar1 in Central Nervous System Disorders and Diseases.Frontiers in neuroscience · 2021Review
- Neuroinflammation and Central Sensitization in Chronic and Widespread Pain.Anesthesiology · 2018Review
- Recent Progress in Understanding the Mechanisms of Pain and Itch: the Second Special Issue.Neuroscience bulletin · 2018Article
- Expression and Role of Voltage-Gated Sodium Channels in Human Dorsal Root Ganglion Neurons with Special Focus on Nav1.7, Species Differences, and Regulation by Paclitaxel.Neuroscience bulletin · 2018Article
- Differential Inhibition of Nav1.7 and Neuropathic Pain by Hybridoma-Produced and Recombinant Monoclonal Antibodies that Target Nav1.7 : Differential activities of Nav1.7-targeting monoclonal antibodies.Neuroscience bulletin · 2018Article
- Lysophosphatidic Acid and Ion Channels as Molecular Mediators of Pain.Frontiers in molecular neuroscience · 2018Review
- Upregulation of Spinal Voltage-Dependent Anion Channel 1 Contributes to Bone Cancer Pain Hypersensitivity in Rats.Neuroscience bulletin · 2017Article
- Protein Kinase C Mediates the Corticosterone-induced Sensitization of Dorsal Root Ganglion Neurons Innervating the Rat Stomach.Journal of neurogastroenterology and motility · 2017Article
- Alpha-lipoic Acid suppresses P2X receptor activities and visceral hypersensitivity to colorectal distention in diabetic rats.Scientific reports · 2017Article
- Up-regulation of CXCR4 expression contributes to persistent abdominal pain in rats with chronic pancreatitis.Molecular pain · 2017Article
- Overexpression of suppressor of cytokine signaling 3 in dorsal root ganglion attenuates cancer-induced pain in rats.Molecular pain · 2017Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Given that lysophosphatidic acid (LPA) and the tetrodotoxin-resistant sodium channel Nav1.8 are both involved in bone cancer pain, the present study was designed to investigate whether crosstalk between the LPA receptor LPA1 (also known as EDG2) and Nav1.8 in the dorsal root ganglion (DRG) contributes to the induction of bone cancer pain. We showed that the EDG2 antagonist Ki16198 blocked the mechanical allodynia induced by intrathecal LPA in naïve rats and attenuated mechanical allodynia in a rat model of bone cancer. EDG2 and Nav1.8 expression in L4-6 DRGs was upregulated following intrathecal or hindpaw injection of LPA. EDG2 and Nav1.8 expression in ipsilateral L4-6 DRGs increased with the development of bone cancer. Furthermore, we showed that EDG2 co-localized with Nav1.8 and LPA remarkably enhanced Nav1.8 currents in DRG neurons, and this was blocked by either a protein kinase C (PKC) inhibitor or a PKCε inhibitor. Overall, we demonstrated the modulation of Nav1.8 by LPA in DRG neurons, and that this probably underlies the peripheral mechanism by which bone cancer pain is induced.
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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.