ArticleFrontiers in immunology2021
HMGB1 Promotes the Release of Sonic Hedgehog From Astrocytes.
Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 19 citations in OpenAlex.
- High mobility group box 1 and its post-translational modifications: Molecular mechanisms underlying neurodegenerative disease pathogenesis.Neural regeneration research · 2026Article
- Proteomic Profiling of Optic Nerves From SMOX-Deficient Mice Identifies Regulators of Neuroinflammation and Axonal Damage in Optic Neuritis.Investigative ophthalmology & visual science · 2026Article
- NMI promotes the secretion of IL-17 and exacerbates psoriasis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Targeting HMGB1 in Microglia Alleviates Neuroinflammation and Modulates the Pro-/Anti-inflammatory Balance of Microglia/Macrophages in Experimental Autoimmune Encephalomyelitis.Molecular neurobiology · 2026Article
- Promoting the nuclear retention of HMGB1 attenuates astrocyte senescence.Journal of neuroinflammation · 2026Article
- Anti-HMGB1 Antibody Therapy Ameliorates Spinal Cord Ischemia-Reperfusion Injury in Rabbits.International journal of molecular sciences · 2025Article
- Pathological role of RAGE underlying progression of various diseases: its potential as biomarker and therapeutic target.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Astrocyte-mediated inflammatory responses in traumatic brain injury: mechanisms and potential interventions.Frontiers in immunology · 2025Review
- Astrocyte Involvement in Blood-Brain Barrier Function: A Critical Update Highlighting Novel, Complex, Neurovascular Interactions.International journal of molecular sciences · 2023Review
- Neural stem cells and oligodendrocyte progenitor cells compete for remyelination in the corpus callosum.Frontiers in cellular neuroscience · 2023Article
- Role of RAGE in the Pathogenesis of Neurological Disorders.Neuroscience bulletin · 2022Review
- Role of high mobility group box protein 1 in depression: A mechanistic and therapeutic perspective.World journal of psychiatry · 2022Review
- Sonic Hedgehog Promotes Proliferation and Migration of Fibroblast-Like Synoviocytes in Rheumatoid Arthritis via Rho/ROCK Signaling.Journal of immunology research · 2022Article
- HMGB1 in nervous system diseases: A common biomarker and potential therapeutic target.Frontiers in neurology · 2022Review
- CB2R Activation Regulates TFEB-Mediated Autophagy and Affects Lipid Metabolism and Inflammation of Astrocytes in POCD.Frontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
13 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High mobility group box 1 protein (HMGB1) is known to be a trigger of inflammation in experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS). However, it may play a different role in some way. Here we investigated the effect of HMGB1 on promoting sonic hedgehog (shh) release from astrocytes as well as the possible signal pathway involved in it. Firstly, shh increased in astrocytes after administration of recombinant HMGB1 or decreased after HMGB1 was blocked when stimulated by homogenate of the onset stage of EAE. Moreover, the expression of HMGB1 receptors, toll-like receptor (TLR) 2 and receptor for advanced glycation end products (RAGE) increased after HMGB1 administration in primary astrocytes. However, the enhancing effect of HMGB1 on shh release from astrocytes was suppressed only after RAGE was knocked out or blocked. Mechanistically, HMGB1 functioned by activating RAGE-mediated JNK, p38, stat3 phosphorylation. Moreover, HMGB1 could induce shh release in EAE. Additionally, intracerebroventricular injection of recombinant shh protein on the onset stage of EAE alleviated the progress of disease and decreased demylination, compared to the mice with normal saline treatment. Overall, HMGB1 promoted the release of shh from astrocytes through signal pathway JNK, p38 and stat3 mediated by receptor RAGE, which may provide new insights of HMGB1 function in EAE.
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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.