ArticlePain research & management2019
P2Y6 Receptor-Mediated Spinal Microglial Activation in Neuropathic Pain.
Article in Pain research & management, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- P2Y6 receptor in the superior cervical ganglion: a key mediator of post-myocardial ischemic sympathetic hyperexcitability via NF-κB mediated neuroinflammation.Purinergic signalling · 2026Article
- Adrenergic Control of P2Y6 Receptor-Dependent Phagocytosis in Rodent and Human Microglia.Glia · 2025Article
- Inhibition of P2Y6 Receptor-Mediated Microglia Phagocytosis Aggravates Brain Injury in Mice of Intracerebral Hemorrhage.Cellular and molecular neurobiology · 2025Article
- Modification of Neural Circuit Functions by Microglial P2Y6 Receptors in Health and Neurodegeneration.Molecular neurobiology · 2025Review
- Inhibition of the Notch Pathway Alleviates Nab-Paclitaxel-Induced Peripheral Neuropathic Pain in Rats by Suppressing HMGB1/Caveolin-1 Signaling in the Spinal Cord.Mediators of inflammation · 2025Article
- The microglial P2YTranslational neurodegeneration · 2024Review
- Functionalized Congeners of 2Cells · 2024Article
- Soluble Epoxide Hydrolase Inhibitor TPPU Alleviates Nab-Paclitaxel-Induced Peripheral Neuropathic Pain via Suppressing NF-Pain research & management · 2023Article
- Synthesis and pharmacological characterization of multiply substituted 2H-chromene derivatives as P2YBioorganic & medicinal chemistry letters · 2022Article
- Overexpression of GRK6 alleviates chronic visceral hypersensitivity through downregulation of P2Y6 receptors in anterior cingulate cortex of rats with prenatal maternal stress.CNS neuroscience & therapeutics · 2022Article
- Structure activity relationship of 3-nitro-2-(trifluoromethyl)-2H-chromene derivatives as P2YBioorganic & medicinal chemistry letters · 2021Article
- Review
- Article
- Experimental Characterization of the Chronic Constriction Injury-Induced Neuropathic Pain Model in Mice.Neurochemical research · 2019Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: To explore the role of purine family member P2Y6 receptors in regulating neuropathic pain (NP) via neuroinflammation in the spinal cord. Methods: Chronic constriction injury of the sciatic nerve (CCI) of NP was classic in setting up models on Sprague-Dawley (SD) rats. Experiments were performed on rats with sham surgery, CCI, CCI + MRS2578 (a P2Y6 receptor antagonist), and UDP (a P2Y6 receptor agonist). The hyperalgesia intensity was mirrored by paw withdrawal threshold (PWT) and thermal withdrawal latency (TWL). Immunofluorescence staining and western blot were used to evaluate activated microglial marker Iba-1. Enzyme-linked immunosorbent assay (ELISA) was used to access levels of IL-6. Conventional reverse transcription polymerase chain reaction (RT-PCR) and western blot analysis were used to detect the expression of P2Y6 mRNA and activation of JAK/STAT signaling. Results: Among all groups, CCI caused decreased PWT and TWL compared to sham surgery, meaning a successful establishment of the NP model. These decreased values of PWT and TWL tests could be prevented by intraperitoneally injected MRS2578 and enhanced by UDP administration. Similarly, CCI induced increase of Iba-1 protein, P2Y6 mRNA expression, and circulating IL-6 secretion, as well as increased JAK2/STAT3 mRNA expression and phosphorylating modification in spinal cord tissues could also be diminished by MRS2578 treatment and exacerbated by UDP. Conclusions: These findings indicated the crucial role of the P2Y6 receptor in modulating the microglial and inflammatory responses in the process of NP
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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.