ArticleProceedings of the National Academy of Sciences of the United States of America2017
High-mobility group box-1 as an autocrine trophic factor in white matter stroke.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. 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, 30 citations in OpenAlex.
- PHGDH-mediated serine synthesis reduces oligodendrocyte death by sustaining GSH and NADPH levels after brain ischemia.Frontiers in pharmacology · 2026Article
- Oligodendrocyte Precursor Cell-Specific HMGB1 Knockout Reduces Immune Cell Infiltration and Demyelination in Experimental Autoimmune Encephalomyelitis Models.Neuroscience bulletin · 2025Article
- HMGB1: A New Target for Ischemic Stroke and Hemorrhagic Transformation.Translational stroke research · 2025Review
- Neuroprotective Potential of Glycyrrhizic Acid in Ischemic Stroke: Mechanisms and Therapeutic Prospects.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Article
- HMGB1, angel or devil, in ischemic stroke.Brain and behavior · 2023Review
- Transcriptional changes in the rat brain induced by repetitive transcranial magnetic stimulation.Frontiers in human neuroscience · 2023Article
- Modeling subcortical ischemic white matter injury in rodents: unmet need for a breakthrough in translational research.Neural regeneration research · 2021Article
- Disulfide HMGB1 acts via TLR2/4 receptors to reduce the numbers of oligodendrocyte progenitor cells after traumatic injury in vitro.Scientific reports · 2021Article
- The Roles of High Mobility Group Box 1 in Cerebral Ischemic Injury.Frontiers in cellular neuroscience · 2020Review
- High-Mobility Group Box 1 Neutralization Prevents Chronic Cerebral Hypoperfusion-Induced Optic Tract Injuries in the White Matter Associated with Down-regulation of Inflammatory Responses.Cellular and molecular neurobiology · 2019Article
- Neuroinflammation: friend and foe for ischemic stroke.Journal of neuroinflammation · 2019Review
- Anti-inflammatory Effects of Traditional Chinese Medicines on PreclinicalFrontiers in pharmacology · 2019Review
- Detrimental Effects of HMGB-1 Require Microglial-Astroglial Interaction: Implications for the Status Epilepticus -Induced Neuroinflammation.Frontiers in cellular neuroscience · 2019Article
- The Role of High Mobility Group Box 1 in Ischemic Stroke.Frontiers in cellular neuroscience · 2019Review
- Danger signals in stroke and their role on microglia activation after ischemia.Therapeutic advances in neurological disorders · 2018Review
- Dysregulation of Astrocytic HMGB1 Signaling in Amyotrophic Lateral Sclerosis.Frontiers in neuroscience · 2018Article
- Toll-like Receptor 2: A Novel Therapeutic Target for Ischemic White Matter Injury and Oligodendrocyte Death.Experimental neurobiology · 2017Review
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
Maintenance of white matter integrity in health and disease is critical for a variety of neural functions. Ischemic stroke in the white matter frequently results in degeneration of oligodendrocytes (OLs) and myelin. Previously, we found that toll-like receptor 2 (TLR2) expressed in OLs provides cell-autonomous protective effects on ischemic OL death and demyelination in white matter stroke. Here, we identified high-mobility group box-1 (HMGB1) as an endogenous TLR2 ligand that promotes survival of OLs under ischemic stress. HMGB1 rapidly accumulated in the culture medium of OLs exposed to oxygen-glucose deprivation (OGD). This conditioned medium exhibited a protective activity against ischemic OL death that was completely abolished by immunodepletion of HMGB1. Knockdown of HMGB1 or application of glycyrrhizin, a specific HMGB1 inhibitor, aggravated OGD-induced OL death, and recombinant HMGB1 application reduced the extent of OL death in a TLR2-dependent manner. We confirmed that cytosolic translocation of HMGB1 and activation of TLR2-mediated signaling pathways occurred in a focal white matter stroke model induced by endothelin-1 injection. Animals with glycyrrhizin coinjection showed an expansion of the demyelinating lesion in a TLR2-dependent manner, accompanied by aggravation of sensorimotor behavioral deficits. These results indicate that HMGB1/TLR2 activates an autocrine trophic signaling pathways in OLs and myelin to maintain structural and functional integrity of the white matter under ischemic conditions.
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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.