ArticlePain2018
Chemokine CCL2 and its receptor CCR2 in the dorsal root ganglion contribute to oxaliplatin-induced mechanical hypersensitivity.
Article in Pain, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
What it found
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The trial behind it
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Who cites it
58 citing papers in PubMed, 100 citations in OpenAlex.
- Nucleolin promotes neuropathic pain by increasing chromatin accessibility at the Ccl2 promoter in primary sensory neurons.Brain, behavior, and immunity · 2026Article
- Skin-resident Langerhans cells drive neuropathic pain via chemokine-dependent neuron-immune communication.The Journal of clinical investigation · 2026Article
- Deciphering and Targeting the Schwannoma-Neuron-Macrophage Crosstalk for the Treatment of Schwannomatosis and Associated Pain.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- C-C motif chemokine ligand 12 (CCL12) is a critical chemokine driving postoperative pain.Pain · 2026Article
- RNA-binding protein MBNL2 mitigates neuropathic pain after chemotherapy through destabilizing CCR2 expression in primary sensory neurons.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Analysis of the circRNA/lncRNA-miRNA-mRNA Networks of Action of Fire Needle Acupuncture in Relieving Chemotherapy-Induced Neuropathic Pain.Journal of pain research · 2026Article
- Proneurotrophin-3 contributes to chemotherapy-induced neuropathic pain through TrkC-mediated CCL2 elevation in DRG neurons.EMBO reports · 2025Article
- Chemokine CCL2 Mediates Neuroglial Crosstalk and Drives Chronic Pain Pathogenesis.Neuroscience bulletin · 2025Review
- The Antinociceptive Effect of Nicorandil in Neuropathic and Nociceptive Pain is Partially Mediated via TRPV1/Opioidergic Signaling.Molecular neurobiology · 2025Article
- Review
- Innate immunity in chemotherapy-induced peripheral neuropathy: recent advances.Frontiers in pain research (Lausanne, Switzerland) · 2025Review
- Activation of TLR4/CCL2 in Intact Neurons Drives Radicular Injury-Induced Global Nerve Trunk Hypersensitivity in Radiculopathy Preclinical Models.Journal of pain research · 2025Article
- Oxaliplatin-induced neuropathic pain in cancer: animal models and related research progress.Frontiers in pharmacology · 2025Review
- α9-Containing Nicotinic Acetylcholine Receptors Are Required for RgIA-5474 Attenuation of Chemotherapy-Induced Neuropathic Pain.ACS pharmacology & translational science · 2024Article
- Neurotoxicity of the antineoplastic drugs: "Doxorubicin" as an example.Journal of molecular histology · 2024Review
- Development of a 3-dimensional organotypic model with characteristics of peripheral sensory nerves.Cell reports methods · 2024Article
- HDAC inhibitors as a potential therapy for chemotherapy-induced neuropathic pain.Inflammopharmacology · 2024Review
- NT-3 contributes to chemotherapy-induced neuropathic pain through TrkC-mediated CCL2 elevation in DRG neurons.EMBO reports · 2024Article
- Contributions of neuroimmune interactions to chemotherapy-induced peripheral neuropathy development and its prevention/therapy.Biochemical pharmacology · 2024Review
- Systemic administration of NIS-lncRNA antisense oligonucleotide alleviates neuropathic pain.Neuroscience letters · 2023Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Activation of innate immune mechanisms within the dorsal root ganglion and spinal dorsal horn has been shown to play a key role in the development of neuropathic pain including paclitaxel-related chemotherapy-induced peripheral neuropathy (CIPN). Here, we tested whether similar mechanisms are generalizable to oxaliplatin-induced CIPN. After a single intraperitoneal injection of 3 mg/kg oxaliplatin, mechanical withdrawal threshold and the expression of C-C chemokine ligand 2 (CCL2) and its receptor, CCR2, in the dorsal root ganglion were measured by behavioral testing and immunohistochemical staining, respectively. Mechanical responsiveness increased from the first day after oxaliplatin injection and persisted until day 15, the last day of this experiment. Immunohistochemical showed that the expression of CCL2/CCR2 started to increase by 4 hours after oxaliplatin treatment, was significantly increased at day 4, and then both signals became normalized by day 15. Cotreatment with intrathecal anti-CCL2 antibodies prevented the development of oxaliplatin-induced mechanical hyperresponsiveness, and transiently reversed established hyperalgesia when given 1 week after chemotherapy. This is the first study to demonstrate CCL2/CCR2 signaling in a model of oxaliplatin-related CIPN; and it further shows that blocking of this signal can attenuate the development of oxaliplatin-induced mechanical hyperalgesia. Activation of innate immune mechanisms may therefore be a generalized basis for CIPN irrespective of the specific class of agent.
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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.