ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2017
Autocrine Interleukin-10 Mediates Glucagon-Like Peptide-1 Receptor-Induced Spinal Microglial β-Endorphin Expression.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.
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Who cites it
50 citing papers in PubMed, 1 synthesis or guideline pooled it, 80 citations in OpenAlex.
- Glucagon-like peptide-1 (GLP-1) receptor agonists for headache and pain disorders: a systematic review.The journal of headache and pain · 2024Pooled it
- A new paradigm of bidirectional regulation of the gut-spinal cord axis.Neural regeneration research · 2026Article
- The Pleiotropic Therapeutic Perspectives of GLP-1 and GIP Receptor Agonists in Spinal Cord Injury: A Narrative Review.Molecular neurobiology · 2026Review
- Glucagon-like Peptide-1 Receptor Agonists and Chronic Pain: Preclinical Antinociceptive Mechanisms, Indirect Metabolic-Functional Effects, and Clinical Considerations-A Narrative Review.Journal of clinical medicine · 2026Review
- Immuno-Mechanical Signaling Network Integration in Temporomandibular Joint Pathology: A TMID Conceptual Framework.International journal of molecular sciences · 2026Review
- Beyond diabetes and obesity: GLP-1 receptor agonists in disrupting the vicious cycle of metabolic dysfunction and neuroinflammation.Diabetes, obesity & metabolism · 2026Review
- The excitatory neurotransmitter glutamate and its receptors: the culprits behind neuropathic pain?Frontiers in aging neuroscience · 2026Review
- Roles of glucagon-like peptide 1 receptor agonists in immune cell biology and autoimmune/autoinflammatory diseases.Cell & bioscience · 2025Review
- Glucagon-like peptide-1 receptor agonists in neuropathic pain: hype or hope?The Korean journal of pain · 2025Article
- Microglial Histaminergic Signaling Promotes Interleukin-10 Production and Ameliorates Motor Dysfunction in Parkinson's Disease.Aging and disease · 2025Article
- Incretin-based therapeutics for the treatment of neurodegenerative diseases.Nature metabolism · 2025Review
- Molecular Anatomy of Synaptic and Extrasynaptic Neurotransmission Between Nociceptive Primary Afferents and Spinal Dorsal Horn Neurons.International journal of molecular sciences · 2025Review
- Advances in GLP-1 receptor agonists for pain treatment and their future potential.The journal of headache and pain · 2025 · on this mapReview
- Review
- Immune drivers of pain resolution and protection.Nature immunology · 2024Review
- Role of glucagon-like peptide-1 receptor agonists in Alzheimer's disease and Parkinson's disease.Journal of biomedical science · 2024Review
- GLP-1 and its derived peptides mediate pain relief through direct TRPV1 inhibition without affecting thermoregulation.Experimental & molecular medicine · 2024Article
- Therapeutic Potential of Glucagon-like Peptide-1 Receptor Agonists in Obstructive Sleep Apnea Syndrome Management: A Narrative Review.Diseases (Basel, Switzerland) · 2024Review
- GLP-1 and Its Derived Peptides Mediate Pain Relief Through Direct TRPV1 Inhibition Without Affecting Thermoregulation.Research square · 2024Article
- Revisiting the role of IL-27 in obesity-related metabolic diseases: safeguard or perturbation?Frontiers in immunology · 2024Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The glucagon-like peptide-1 (GLP-1) receptor agonist exenatide stimulates microglial β-endorphin expression and subsequently produces neuroprotection and antinociception. This study illustrated an unrecognized autocrine role of IL-10 in mediation of exenatide-induced β-endorphin expression. Treatment with exenatide in cultured primary spinal microglia concentration dependently stimulated the expression of the M2 microglial markers IL-10, IL-4, Arg 1, and CD206, but not the M1 microglial markers TNF-α, IL-1β, IL-6, or CD68. Intrathecal exenatide injection also significantly upregulated spinal microglial expression of IL-10, IL-4, Arg 1, and CD206, but not TNF-α, IL-1β, IL-6, or CD68. Intrathecal injection of exenatide stimulated spinal microglial expression of IL-10 and β-endorphin in neuropathic rats. Furthermore, treatment with IL-10 (but not IL-4) stimulated β-endorphin expression in cultured primary microglia, whereas treatment with β-endorphin failed to increase IL-10 expression. The IL-10-neutralizing antibody entirely blocked exenatide-induced spinal microglial expression of β-endorphin
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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.