ArticleMolecular pain2014
Lysophosphatidic acid and its receptors LPA1 and LPA3 mediate paclitaxel-induced neuropathic pain in mice.
Article in Molecular pain, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 59 citations in OpenAlex.
- Gintonin prevents paclitaxel-induced neuropathic pain via spinal LPAJournal of ginseng research · 2026Article
- Oxypeucedanin attenuates neuropathic pain in male mice via inhibiting lysophosphatidic acid receptor signaling.iScience · 2026Article
- Unraveling the Role of Autotaxin and Lysophosphatidic Acid in Alzheimer's Disease: From Molecular Mechanisms to Therapeutic Potential.International journal of molecular sciences · 2025Review
- Evaluation and application analysis of animal models of PIPNP based on data mining.Open life sciences · 2025Review
- TLR-4: a promising target for chemotherapy-induced peripheral neuropathy.Molecular biology reports · 2024Review
- The Efficacy of Neuromodulation Interventions for Chemotherapy-Induced Peripheral Neuropathy: A Systematic Review and Meta-Analysis.Journal of pain research · 2024Review
- Fibromyalgia Animal Models Using Intermittent Cold and Psychological Stress.Biomedicines · 2023Review
- Article
- scRNA-seq generates a molecular map of emerging cell subtypes after sciatic nerve injury in rats.Communications biology · 2022Article
- Spatial transcriptomics of dorsal root ganglia identifies molecular signatures of human nociceptors.Science translational medicine · 2022Article
- Lysophosphatidic Acid Induced Apoptosis, DNA Damage, and Oxidative Stress in Spinal Cord Neurons by Upregulating LPA4/LPA6 Receptors.Mediators of inflammation · 2022Article
- A review of applications of metabolomics in osteoarthritis.Clinical rheumatology · 2021Review
- Review
- Diversity of Receptor Expression in Central and Peripheral Mouse Neurons Estimated from Single Cell RNA Sequencing.Neuroscience · 2021Article
- Lysophosphatidic Acid Signalling in Nervous System Development and Function.Neuromolecular medicine · 2021Review
- The Roles of Lpar1 in Central Nervous System Disorders and Diseases.Frontiers in neuroscience · 2021Review
- Blockers of Wnt3a, Wnt10a, or β-Catenin Prevent Chemotherapy-Induced Neuropathic Pain In Vivo.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Article
- BMS-986020, a Specific LPAAntioxidants (Basel, Switzerland) · 2020Article
- Article
- An Investigation of the Molecular Mechanisms Underlying the Analgesic Effect of Jakyak-Gamcho Decoction: A Network Pharmacology Study.Evidence-based complementary and alternative medicine : eCAM · 2020Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPaclitaxel, which is widely used for the treatment of solid tumors, causes neuropathic pain via poorly understood mechanisms. Previously, we have demonstrated that lysophosphatidic acid (LPA) and its receptors (LPA1 and LPA3) are required for the initiation of peripheral nerve injury-induced neuropathic pain. The present study aimed to clarify whether LPA and its receptors could mediate paclitaxel-induced neuropathic pain.
resultsIntraperitoneal administration of paclitaxel triggered a marked increase in production of LPA species (18:1-, 16:0-, and 18:0-LPA) in the spinal dorsal horn. Also, we found significant activations of spinal cytosolic phospholipase A2 and calcium-independent phospholipase A2 after the paclitaxel treatment. The paclitaxel-induced LPA production was completely abolished not only by intrathecal pretreatment with neurokinin 1 (NK1) or N-methyl-D-aspartate (NMDA) receptor antagonist, but also in LPA1 receptor-deficient (Lpar1-/-) and LPA3 receptor-deficient (Lpar3-/-) mice. In addition, the pharmacological blockade of NK1 or NMDA receptor prevented a reduction in the paw withdrawal threshold against mechanical stimulation after paclitaxel treatments. Importantly, the paclitaxel-induced mechanical allodynia was absent in Lpar1-/- and Lpar3-/- mice.
conclusionsThese results suggest that LPA1 and LPA3 receptors-mediated amplification of spinal LPA production is required for the development of paclitaxel-induced neuropathic pain.
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