ArticleBrain, behavior, and immunity2014
Identification of a functional interaction of HMGB1 with Receptor for Advanced Glycation End-products in a model of neuropathic pain.
Article in Brain, behavior, and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 89 citations in OpenAlex.
- Neuro-immune interactions in tumors, immune-related disorders, and infections.Signal transduction and targeted therapy · 2026Review
- The Receptor for Advanced Glycation End-products in the Mouse Anterior Cingulate Cortex is Involved in Neuron‒Astrocyte Coupling in Chronic Inflammatory Pain and Anxiety Comorbidity.Molecular neurobiology · 2025Article
- Neuroimmune Circuits in Allergic Diseases.Annual review of immunology · 2025Review
- Accumulation of advanced oxidative protein products exacerbate satellite glial cells activation and neuropathic pain.Molecular medicine (Cambridge, Mass.) · 2025Article
- Role of pattern recognition receptors in chemotherapy-induced neuropathic pain.Brain : a journal of neurology · 2024Article
- Hmgb1 Silencing in the Amygdala Inhibits Pain-Related Behaviors in a Rat Model of Neuropathic Pain.International journal of molecular sciences · 2023Article
- HMGB1 in depression: An overview of microglial HMBG1 in the pathogenesis of depression.Brain, behavior, & immunity - health · 2023Review
- Propranolol treatment during repetitive mild traumatic brain injuries induces transcriptomic changes in the bone marrow of mice.Frontiers in neuroscience · 2023Article
- Article
- Blocking receptor for advanced glycation end products (RAGE) or toll-like receptor 4 (TLR4) prevents posttraumatic epileptogenesis in mice.Epilepsia · 2021Article
- Sensory Neuron TLR4 mediates the development of nerve-injury induced mechanical hypersensitivity in female mice.Brain, behavior, and immunity · 2021Article
- Spinal Nrf2 translocation may inhibit neuronal NF-κB activation and alleviate allodynia in a rat model of bone cancer pain.Journal of neurochemistry · 2021Article
- HMGB1, NLRP3, IL-6 and ACE2 levels are elevated in COVID-19 with headache: a window to the infection-related headache mechanism.The journal of headache and pain · 2021Article
- LPS Primes Brain Responsiveness to High Mobility Group Box-1 Protein.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Suppression of TLR4-MyD88 signaling pathway attenuated chronic mechanical pain in a rat model of endometriosis.Journal of neuroinflammation · 2021Article
- Modulation of Vagal Sensory NeuronsFrontiers in physiology · 2021Article
- High mobility group box 1 induces bone pain associated with bone invasion in a mouse model of advanced head and neck cancer.Oncology reports · 2020Article
- The alarmins S100A8 and S100A9 mediate acute pain in experimental synovitis.Arthritis research & therapy · 2020Article
- High Mobility Group Box 1 in Human Cancer.Cells · 2020Review
- The innate immune response as a mediator of osteoarthritis pain.Osteoarthritis and cartilage · 2020Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Recent studies indicate that the release of high mobility group box 1 (HMGB1) following nerve injury may play a central role in the pathogenesis of neuropathic pain. HMGB1 is known to influence cellular responses within the nervous system via two distinct receptor families; the Receptor for Advanced Glycation End-products (RAGE) and Toll-like receptors (TLRs). The degree to which HMGB1 activates a receptor is thought to be dependent upon the oxidative state of the ligand, resulting in the functional isoforms of all-thiol HMGB1 (at-HMGB1) acting through RAGE, and disufide HMGB1 (ds-HMGB1) interacting with TLR4. Though it is known that dorsal root ganglia (DRG) sensory neurons exposed to HMGB1 and TLR4 agonists can influence excitation, the degree to which at-HMGB1 signaling through neuronal RAGE contributes to neuropathic pain is unknown. Here we demonstrate that at-HMGB1 activation of nociceptive neurons is dependent on RAGE and not TLR4. To distinguish the possible role of RAGE on neuropathic pain, we characterized the changes in RAGE mRNA expression up to one month after tibial nerve injury (TNI). RAGE mRNA expression in lumbar dorsal root ganglion (DRG) is substantially increased by post-injury day (PID) 28 when compared with sham injured rodents. Protein expression at PID28 confirms this injury-induced event in the DRG. Moreover, a single exposure to monoclonal antibody to RAGE (RAGE Ab) failed to abrogate pain behavior at PID 7, 14 and 21. However, RAGE Ab administration produced reversal of mechanical hyperalgesia on PID28. Thus, at-HMGB1 activation through RAGE may be responsible for sensory neuron sensitization and mechanical hyperalgesia associated with chronic neuropathic pain states.
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Registered trials
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.