ArticleMolecular pain2013
An LPA species (18:1 LPA) plays key roles in the self-amplification of spinal LPA production in the peripheral neuropathic pain model.
Article in Molecular pain, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 60 citations in OpenAlex.
- Lysophosphatidic acid is associated with neuropathic pain intensity in humans: An exploratory study.PloS one · 2018Trial
- Comparative Analysis of Lysophosphatidic Acid Levels in Fibromyalgia and Other Painful Conditions in Female Patients.European journal of pain (London, England) · 2025Article
- Clinical measures in chronic neuropathic pain are related to the Kennedy and endocannabinoid pathways.European journal of clinical investigation · 2025Article
- Daphnetin Ameliorates Neuropathic Pain via Regulation of Microglial Responses and Glycerophospholipid Metabolism in the Spinal Cord.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Discovery of a brain penetrant small molecule antagonist targeting LPA1 receptors to reduce neuroinflammation and promote remyelination in multiple sclerosis.Scientific reports · 2024Article
- Role for CCN1 in lysophosphatidic acid response in PC-3 human prostate cancer cells.Journal of cell communication and signaling · 2024Article
- TMEM120A/TACAN: A putative regulator of ion channels, mechanosensation, and lipid metabolism.Channels (Austin, Tex.) · 2023Review
- Plasma Lysophosphatidic Acid Concentrations in Sex Differences and Psychiatric Comorbidity in Patients with Cocaine Use Disorder.International journal of molecular sciences · 2023Article
- Gintonin, aJournal of ginseng research · 2023Article
- Different Profiles of the Triad of Lysophosphatidylcholine, Lysophosphatidic Acid, and Autotaxin in Patients with Neuropathic Pain Diseases: a Preliminary Observational Study.Pain and therapy · 2022Article
- Elucidating the binding mechanism of LPA species and analogs in an LPAJournal of molecular graphics & modelling · 2022Article
- The LPA-CDK5-tau pathway mediates neuronal injury in an in vitro model of ischemia-reperfusion insult.BMC neurology · 2022Article
- Lysophosphatidic Acid Induced Apoptosis, DNA Damage, and Oxidative Stress in Spinal Cord Neurons by Upregulating LPA4/LPA6 Receptors.Mediators of inflammation · 2022Article
- Lysophosphatidic Acid Signalling in Nervous System Development and Function.Neuromolecular medicine · 2021Review
- Role of lysophosphatidic acid and its receptors in health and disease: novel therapeutic strategies.Signal transduction and targeted therapy · 2021Review
- Conditional Lpar1 gene targeting identifies cell types mediating neuropathic pain.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Pain Control by Targeting Oxidized Phospholipids: Functions, Mechanisms, Perspectives.Frontiers in endocrinology · 2020Review
- Lysophosphatidic acids and their substrate lysophospholipids in cerebrospinal fluid as objective biomarkers for evaluating the severity of lumbar spinal stenosis.Scientific reports · 2019Article
- Effects of the LPAFrontiers in molecular neuroscience · 2019Article
- Matrix-Assisted Laser Desorption Ionization Mapping of Lysophosphatidic Acid Changes after Traumatic Brain Injury and the Relationship to Cellular Pathology.The American journal of pathology · 2018Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundWe previously reported that nerve injury-induced neuropathic pain is initiated by newly produced lysophosphatidic acid (LPA).
resultsIn this study, we developed a quantitative mass spectrometry for detecting LPA species by using Phos-tag. Following nerve injury, the levels of 18:1, 16:0 and 18:0 LPA in the spinal dorsal horn significantly increased at 3 h and declined at 6 h. Among them, 18:1 LPA level was the most abundant. In the same preparation, there were significant elevations in the activities of cytosolic phospholipase A2 (cPLA2) and calcium-independent phospholipase A2 (iPLA2), key enzymes for LPA synthesis, at 1 h, while there was no significant change in phospholipase A1 activity. Pharmacological studies revealed that NMDA and neurokinin 1 receptors, cPLA2, iPLA2 and microglial activation, as well as LPA1 and LPA3 receptors were all involved in the nerve injury-induced LPA production, and underlying cPLA2 and iPLA2 activations. In the cells expressing LPA1 or LPA3 receptor, the receptor-mediated calcium mobilization was most potent with 18:1 LPA, compared with 16:0 or 18:0 LPA. Moreover, the intrathecal injection of 18:1 LPA, but not 16:0 or 18:0 LPA, caused a spinal LPA production and neuropathic pain-like behavior.
conclusionThese results suggest that 18:1 LPA is the predominant ligand responsible for LPA1 and LPA3 receptors-mediated amplification of LPA production through microglial activation.
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