ArticleScientific reports2017
Acute administration of catalase targeted to ICAM-1 attenuates neuropathology in experimental traumatic brain injury.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
What it found
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Who cites it
51 citing papers in PubMed, 72 citations in OpenAlex.
- ICAM-1 targeting of nanocarriers in a human blood-brain-barrier-on-a-chip complementsJournal of drug targeting · 2026Article
- Endothelial ferroptosis in blood-brain barrier dysfunction and neuroinflammation: mechanisms and immune-vascular crosstalk.Frontiers in immunology · 2026Review
- Pathological neural and immune synapses in glioblastoma progression: mechanisms and therapeutic opportunities.Frontiers in neural circuits · 2026Review
- Blood-Based Biomarkers for Traumatic Brain Injury: A New Era in Diagnosis and Prognosis.International journal of molecular sciences · 2025Review
- Endothelial dysfunction in acute ischemic stroke: a review.Journal of neurology · 2025Review
- The role of Panax notoginseng saponins in cerebrovascular neurological disorders: an overview of mechanisms and functions.Frontiers in pharmacology · 2025Review
- The role of reactive oxygen species in the regulation of the blood-brain barrier.Tissue barriers · 2025Review
- New Cellular Models to Support Preclinical Studies on ICAM-1-Targeted Drug Delivery.Journal of drug delivery science and technology · 2024Article
- Review
- Reprograming Clots for In Vivo Chemical Targeting in Traumatic Brain Injury.Advanced materials (Deerfield Beach, Fla.) · 2024Article
- ICAM-1 Deletion Using CRISPR/Cas9 Protects the Brain from Traumatic Brain Injury-Induced Inflammatory Leukocyte Adhesion and Transmigration Cascades by Attenuating the Paxillin/FAK-Dependent Rho GTPase Pathway.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Engineered Dual Antioxidant Enzyme Complexes Targeting ICAM-1 on Brain Endothelium Reduce Brain Injury-Associated Neuroinflammation.Bioengineering (Basel, Switzerland) · 2024Article
- Mild traumatic brain injury in Drosophila melanogaster alters reactive oxygen and nitrogen species in a sex-dependent manner.Experimental neurology · 2024Article
- Activation of CB2R by synthetic CB2R agonist, PM289, improves brain endothelial barrier properties, decreases inflammatory response and enhances endothelial repair.NeuroImmune pharmacology and therapeutics · 2023Article
- Antioxidant theranostic copolymer-mediated reduction in oxidative stress following traumatic brain injury improves outcome in a mouse model.Advanced therapeutics · 2023Article
- Therapeutic Investigation of Palm Oil Mill Effluent-Derived Beta-Carotene in Streptozotocin-Induced Diabetic Retinopathy via the Regulation of Blood-Retina Barrier Functions.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Sex-based differences of antioxidant enzyme nanoparticle effects following traumatic brain injury.Journal of controlled release : official journal of the Controlled Release Society · 2023Article
- Ferroptosis and mitochondrial dysfunction in acute central nervous system injury.Frontiers in cellular neuroscience · 2023Review
- Article
- What Happens in TBI? A Wide Talk on Animal Models and Future Perspective.Current neuropharmacology · 2023Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Traumatic brain injury (TBI) contributes to one third of injury related deaths in the US. Treatment strategies for TBI are supportive, and the pathophysiology is not fully understood. Secondary mechanisms of injury in TBI, such as oxidative stress and inflammation, are points at which intervention may reduce neuropathology. Evidence suggests that reactive oxygen species (ROS) propagate blood-brain barrier (BBB) hyperpermeability and inflammation following TBI. We hypothesized that targeted detoxification of ROS may improve the pathological outcomes of TBI. Following TBI, endothelial activation results in a time dependent increase in vascular expression of ICAM-1. We conjugated catalase to anti-ICAM-1 antibodies and administered the conjugate to 8 wk old C57BL/6J mice 30 min after moderate controlled cortical impact injury. Results indicate that catalase targeted to ICAM-1 reduces markers of oxidative stress, preserves BBB permeability, and attenuates neuropathological indices more effectively than non-targeted catalase and anti-ICAM-1 antibody alone. Furthermore, the study of microglia by two-photon microscopy revealed that anti-ICAM-1/catalase prevents the transition of microglia to an activated phenotype. These findings demonstrate the use of a targeted antioxidant enzyme to interfere with oxidative stress mechanisms in TBI and provide a proof-of-concept approach to improve acute TBI management that may also be applicable to other neuroinflammatory conditions.
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Registered trials
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