ArticleJournal of neuropathology and experimental neurology2016
HMGB1 Translocation After Ischemia in the Ovine Fetal Brain.
Article in Journal of neuropathology and experimental neurology, 2016. 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, 21 citations in OpenAlex.
- Lactylation of HMGB1 at K177 Drives Nuclear Export of TIAR to Promote Hypoxia-Induced Stress Granule Formation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- 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
- Prognostic value of serum high-mobility group box 1 in neonates with neonatal encephalopathy.Pediatric research · 2025Article
- 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
- Disulfide HMGB1 acts via TLR2/4 receptors to reduce the numbers of oligodendrocyte progenitor cells after traumatic injury in vitro.Scientific reports · 2021Article
- N-Acetyl Cysteine Restores Sirtuin-6 and Decreases HMGB1 Release Following Lipopolysaccharide-Sensitized Hypoxic-Ischemic Brain Injury in Neonatal Mice.Frontiers in cellular neuroscience · 2021Article
- Novel Neuroprotective Agents to Treat Neonatal Hypoxic-Ischemic Encephalopathy: Inter-Alpha Inhibitor Proteins.International journal of molecular sciences · 2020Review
- The Roles of High Mobility Group Box 1 in Cerebral Ischemic Injury.Frontiers in cellular neuroscience · 2020Review
- Inter-alpha Inhibitor Proteins Modulate Neuroinflammatory Biomarkers After Hypoxia-Ischemia in Neonatal Rats.Journal of neuropathology and experimental neurology · 2019Article
- High-mobility group box-1 translocation and release after hypoxic ischemic brain injury in neonatal rats.Experimental neurology · 2019Article
- High-Mobility Group Box 1 Contributes to Cerebral Cortex Injury in a Neonatal Hypoxic-Ischemic Rat Model by Regulating the Phenotypic Polarization of Microglia.Frontiers in cellular neuroscience · 2019Article
- Anti-Cytokine Therapy to Attenuate Ischemic-Reperfusion Associated Brain Injury in the Perinatal Period.Brain sciences · 2018Review
- Location, Location, Location: Appraising the Pleiotropic Function of HMGB1 in Fetal Brain.Journal of neuropathology and experimental neurology · 2017Article
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12 authors at 4 institutions in 2 countries.
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Abstract
Inflammation contributes to the evolution of hypoxic-ischemic (HI) brain injury. High-mobility group box-1 (HMGB1) is a nuclear protein that is translocated from the nucleus and released after ischemia in adult rodents and thereby initiates inflammatory responses. However, there is very little information regarding the effects of HI on HMGB1 in immature brains. To investigate the effects of HI on HMGB1 in the term-equivalent fetal brain, ovine fetuses at 127 days gestation were studied after 30 minutes of carotid occlusion. Groups were sham-control and ischemia with 48 hours and ischemia with 72 hours of reperfusion. By immunohistochemistry, HMGB1 was found to be localized primarily in cell nuclei and partially in cytoplasmic compartments in the cerebral cortex of controls. Ischemia increased the area fraction of neuronal cells with cytoplasmic HMGB1 staining, and Western immunoblot revealed that cytosolic HMGB1 expression increased after ischemia (p < 0.05) and decreased in nuclei in ischemic versus the sham-control brains (p < 0.05). These data indicate that HMGB1 translocates from the nuclear to cytosolic compartments after ischemic brain injury in fetal sheep. This translocation may enable the action of HMGB1 as a proinflammatory cytokine that contributes to HI injury in the developing brain.
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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.