ArticleExperimental neurology2019
High-mobility group box-1 translocation and release after hypoxic ischemic brain injury in neonatal rats.
Article in Experimental neurology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 42 citations in OpenAlex.
- Blood-Based Biomarkers for Post-Stroke Cognitive Impairment.Current issues in molecular biology · 2026Review
- Systemic Inflammation and Central Neuronal Damage: The Relationship Between Neutrophil-to-Lymphocyte Ratio and Neuron-Specific Enolase in Acute Ischemic Stroke.Immunity, inflammation and disease · 2026Article
- The Dynamics of Neuroinflammation in Traumatic Brain Injury: Molecular Markers Useful for Establishing the Post-Traumatic Interval in Forensic Practice.International journal of molecular sciences · 2026Review
- Novel purine derivatives mitigate hypoxia ischemia related brain injury through agrin, zyxin and synaptotagmin proteins.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- Novel peptidomimetic compounds attenuate hypoxic-ischemic brain injury in neonatal rats.Experimental neurology · 2025Article
- Prognostic value of serum high-mobility group box 1 in neonates with neonatal encephalopathy.Pediatric research · 2025Article
- Activation of the LKB1/AMPK/HIF-1α Pathway by Metformin to Promote Neovascularisation in Cerebral Ischaemia.Neurochemical research · 2024Article
- The Neuroprotective Mechanisms of PPAR-γ: Inhibition of Microglia-Mediated Neuroinflammation and Oxidative Stress in a Neonatal Mouse Model of Hypoxic-Ischemic White Matter Injury.CNS neuroscience & therapeutics · 2024Article
- N-acetylserotonin alleviates retinal ischemia-reperfusion injuryInternational journal of ophthalmology · 2024Article
- Circulating HMGB1 in acute ischemic stroke and its association with post-stroke cognitive impairment.PeerJ · 2024Article
- ADAMTS-13 and HMGB1-induced oxidative stress in Taenia multiceps-infected animals.Scientific reports · 2023Article
- Inter-Alpha Inhibitor Proteins Modify the Microvasculature after Exposure to Hypoxia-Ischemia and Hypoxia in Neonatal Rats.International journal of molecular sciences · 2023Article
- Ferroptosis: A Promising Therapeutic Target for Neonatal Hypoxic-Ischemic Brain Injury.International journal of molecular sciences · 2022Review
- Time Course of Changes in the Neurovascular Unit after Hypoxic-Ischemic Injury in Neonatal Rats.International journal of molecular sciences · 2022Article
- Inter-alpha Inhibitor Proteins Ameliorate Brain Injury and Improve Behavioral Outcomes in a Sex-Dependent Manner After Exposure to Neonatal Hypoxia Ischemia in Newborn and Young Adult Rats.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022Article
- The Regulatory Effects of Traditional Chinese Medicine on Ferroptosis.Oxidative medicine and cellular longevity · 2022Review
- Glycyrrhizin Attenuates Hypoxic-Ischemic Brain Damage by Inhibiting Ferroptosis and Neuroinflammation in Neonatal Rats via the HMGB1/GPX4 Pathway.Oxidative medicine and cellular longevity · 2022Article
- Changes in Cellular Localization of Inter-Alpha Inhibitor Proteins after Cerebral Ischemia in the Near-Term Ovine Fetus.International journal of molecular sciences · 2021Article
- High mobility group box-1 protein as a therapeutic target in perinatal hypoxic-ischemic brain injury.Neural regeneration research · 2021Article
- Hypoxia and oxidative stress induce sterile placental inflammation in vitro.Scientific reports · 2021Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Inflammation contributes to neonatal brain injury. Pro-inflammatory cytokines represent key inflammatory meditators in neonatal hypoxic-ischemic (HI) brain injury. The high mobility group box-1 (HMGB1) protein is a nuclear protein with pro-inflammatory cytokine properties when it is translocated from the nucleus and released extracellularly after stroke in adult rodents. We have previously shown that HMGB1 is translocated from the nucleus to cytosolic compartment after ischemic brain injury in fetal sheep. In the current study, we utilized the Rice-Vannucci model to investigate the time course of HMGB1 translocation and release after HI injury in neonatal rats. HMGB1 was located in cellular nuclei of brains from sham control rats. Nuclear to cytoplasmic translocation of HMGB1 was detected in the ipsilateral-HI hemisphere as early as zero h after HI, and released extracellularly as early as 6 h after HI. Immunohistochemical double staining detected HMGB1 translocation mainly in neurons along with release from apoptotic cells after HI. Serum HMGB1 increased at 3 h and decreased by 24 h after HI. In addition, rat brains exposed to hypoxic injury alone also exhibited time dependent HMGB1 translocation at 3, 12 and 48 h after hypoxia. Consequently, HMGB1 responds similarly after HI injury in the brains of neonatal and adult subjects. We conclude that HMGB1 is sensitive early indicator of neonatal HI and hypoxic brain injury.
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