ArticleThe Journal of biological chemistry2012
Targeted deletion of LPA5 identifies novel roles for lysophosphatidic acid signaling in development of neuropathic pain.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 126 citations in OpenAlex.
- LPA4 in the spinal dorsal horn is a potential therapeutic target for inflammatory pain and neuropathic mechanical hypersensitivity.iScience · 2026Article
- Lysophosphatidic Acid Receptor 5 (LPAInternational journal of molecular sciences · 2026Article
- LPA/LPAR signaling drives temporomandibular disorders-like pain through regulating the expression and sensitization of PIEZO2.Science advances · 2026Article
- Exosomes: Roles and Therapeutic Potential in Pain.Biomedicines · 2026Review
- Lysophosphatidic acid receptor 5 in insular cortex as a potential analgesic target in neuropathic pain.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- Unraveling the Role of Autotaxin and Lysophosphatidic Acid in Alzheimer's Disease: From Molecular Mechanisms to Therapeutic Potential.International journal of molecular sciences · 2025Review
- Lysophosphatidic Acid Receptors LPAR5 and LPAR2 Inversely Control Hydroxychloroquine-Evoked Itch and Scratching in Mice.International journal of molecular sciences · 2024Article
- Lysophospholipid receptors in neurodegeneration and neuroprotection.Exploration of neuroprotective therapy · 2024Article
- Autotaxin-lysophosphatidic acid receptor 5 axis evokes endothelial dysfunction via reactive oxygen species signaling.Experimental biology and medicine (Maywood, N.J.) · 2023Article
- Emerging Roles of Lysophosphatidic Acid in Macrophages and Inflammatory Diseases.International journal of molecular sciences · 2023Review
- Emerging roles of lysophosphatidic acid receptor subtype 5 (LPAR5) in inflammatory diseases and cancer.Pharmacology & therapeutics · 2023Review
- Editorial: Women in science: pharmacological treatment of pain.Frontiers in pain research (Lausanne, Switzerland) · 2023Article
- Isoquinolone derivatives as lysophosphatidic acid receptor 5 (LPA5) antagonists: Investigation of structure-activity relationships, ADME properties and analgesic effects.European journal of medicinal chemistry · 2022Article
- GPR92 activation in islet macrophages controls β cell function in a diet-induced obesity model.The Journal of clinical investigation · 2022Article
- Compensatory Upregulation of LPACells · 2022Article
- Lysophosphatidic Acid Receptor 5 (LPACells · 2022Article
- An LPARFrontiers in pain research (Lausanne, Switzerland) · 2022Article
- Survival of Stem Cells and Progenitors in the Intestine Is Regulated by LPACellular and molecular gastroenterology and hepatology · 2022Article
- Endocannabinoid signaling pathways: beyond CB1R and CB2R.Journal of cell communication and signaling · 2021Review
- Generation of an Lpar1-EGFP Fusion Knock-in Transgenic Mouse Line.Cell biochemistry and biophysics · 2021Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Lysophosphatidic acid (LPA) is a bioactive lipid that serves as an extracellular signaling molecule acting through cognate G protein-coupled receptors designated LPA(1-6) that mediate a wide range of both normal and pathological effects. Previously, LPA(1), a G(αi)-coupled receptor (which also couples to other G(α) proteins) to reduce cAMP, was shown to be essential for the initiation of neuropathic pain in the partial sciatic nerve ligation (PSNL) mouse model. Subsequent gene expression studies identified LPA(5), a G(α12/13)- and G(q)-coupled receptor that increases cAMP, in a subset of dorsal root ganglion neurons and also within neurons of the spinal cord dorsal horn in a pattern complementing, yet distinct from LPA(1), suggesting its possible involvement in neuropathic pain. We therefore generated an Lpar5 null mutant by targeted deletion followed by PSNL challenge. Homozygous null mutants did not show obvious base-line phenotypic defects. However, following PSNL, LPA(5)-deficient mice were protected from developing neuropathic pain. They also showed reduced phosphorylated cAMP response element-binding protein expression within neurons of the dorsal horn despite continued up-regulation of the characteristic pain-related markers Caα(2)δ(1) and glial fibrillary acidic protein, results that were distinct from those previously observed for LPA(1) deletion. These data expand the influences of LPA signaling in neuropathic pain through a second LPA receptor subtype, LPA(5), involving a mechanistically distinct downstream signaling pathway compared with LPA(1).
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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.