ArticleJournal of neuroinflammation2021
Anti-AQP4 autoantibodies promote ATP release from astrocytes and induce mechanical pain in rats.
Article in Journal of neuroinflammation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 50 citations in OpenAlex.
- Progress on experimental models of neuromyelitis optica spectrum disease.IBRO neuroscience reports · 2026Review
- Autoantibodies as drivers of neuropathic pain.Trends in molecular medicine · 2026Review
- Serum Aquaporin-4 Antibody Status and TGF-β in Neuromyelitis Optica Spectrum Disorder: Impact on Astrocyte Function and Correlation with Disease Activity and Severity.Neurology international · 2025Article
- Inflammatory transcriptomic signatures in a human cellular NMOSD model reveal upregulation of NF-κB and IL6 pathways.Scientific reports · 2025Article
- Spinal astrocytes involved in the pathogenesis and treatment of neuropathic pain.Frontiers in cellular neuroscience · 2025Review
- B cells drive neuropathic pain-related behaviors in mice through IgG-Fc gamma receptor signaling.Science translational medicine · 2024Article
- Article
- Elucidating the mechanisms underlying astrocyte-microglia crosstalk in hippocampal neuroinflammation induced by acute diquat exposure.Environmental science and pollution research international · 2024Article
- Scientific issues with rodent models of neuromyelitis optic spectrum disorders.Frontiers in immunology · 2024Review
- Increased Cerebrospinal Fluid Adenosine 5'-Triphosphate Levels in Patients with Guillain-Barré Syndrome and Chronic Inflammatory Demyelinating Polyneuropathy.Neurology research international · 2024Article
- AQP4 is an Emerging Regulator of Pathological Pain: A Narrative Review.Cellular and molecular neurobiology · 2023Review
- Autoimmune-mediated astrocytopathy.Inflammation and regeneration · 2023Review
- The circadian regulation of extracellular ATP.Purinergic signalling · 2023Review
- Central nervous system demyelinating diseases: glial cells at the hub of pathology.Frontiers in immunology · 2023Review
- Enhanced nociceptive behavior and expansion of associated primary afferents in a rabbit model of cerebral palsy.Journal of neuroscience research · 2022Article
- Targeting choroid plexus epithelium as a novel therapeutic strategy for hydrocephalus.Journal of neuroinflammation · 2022Review
- The autoimmune aetiology of unexplained chronic pain.Autoimmunity reviews · 2022Review
- The role of astrocytes in neuropathic pain.Frontiers in molecular neuroscience · 2022Review
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Authors and funding
19 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundIntractable neuropathic pain is a common symptom of neuromyelitis optica spectrum disorder (NMOSD). However, the underlying mechanism of NMOSD pain remains to be elucidated. In this study, we focused on ATP, which is one of the damage-associated molecular patterns, and also a well-recognized molecule involved in peripheral neuropathic pain.
methodsWe assessed the development of pain symptoms by injecting anti-AQP4 recombinant autoantibodies (rAQP4 IgG) into rat spinal cords. We incubated HEK293 cells expressing AQP4 (HEK-AQP4) and rat astrocytes with rAQP4 IgG and assessed the level of ATP in the supernatant. We performed transcriptome analysis of the spinal cords injected with rAQP4 IgG. Pharmacological inhibition was also applied to investigate the involvement of ATP in the development of neuropathic pain in our rat model. The ATP concentration within the cerebrospinal fluid was examined in patients with NMOSD and other neurological diseases.
resultsDevelopment of mechanical allodynia was confirmed in rAQP4 IgG-treated rats. AQP4-Ab-mediated extracellular ATP release from astrocytes was observed in vitro, and pharmacological inhibition of ATP receptor reversed mechanical allodynia in the rAQP4 IgG-treated rats. Furthermore, transcriptome analysis revealed elevation of gene expressions related to several ATP receptors including P2rx4 and IL1B in the spinal cord of rAQP4 IgG-treated rats. In patients, CSF ATP concentration was significantly higher in the acute and remission phase of NMOSD than in multiple sclerosis or other neurological disorders.
conclusionAnti-AQP4 antibody was shown to induce the release of extracellular ATP from astrocytes. The ATP-mediated development of mechanical allodynia was also suggested in rats treated with anti-AQP4 antibody. Our study indicates the pivotal role of ATP in the pain mechanism of NMOSD.
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