ArticleCell death & disease2018
EphB3 signaling induces cortical endothelial cell death and disrupts the blood-brain barrier after traumatic brain injury.
Article in Cell death & disease, 2018. 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.
- Pathological Roles of Astrocytes in Traumatic Brain Injury.CNS neuroscience & therapeutics · 2026Review
- Cognitive loss after brain trauma results from sex-specific activation of synaptic pruning processes.Brain : a journal of neurology · 2026Article
- Activation of multiple Eph receptors on neuronal membranes correlates with the onset of optic neuropathy.Eye and vision (London, England) · 2023Article
- Deep sequencing of circulating miRNAs and target mRNAs level in deep venous thrombosis patients.IET systems biology · 2023Article
- Activation of Multiple Eph Receptors on Neuronal Membranes Correlates with The Onset of Traumatic Optic Neuropathy.bioRxiv : the preprint server for biology · 2023Article
- Establishing a prediction model of severe acute mountain sickness using machine learning of support vector machine recursive feature elimination.Scientific reports · 2023Article
- Electroacupuncture alleviates traumatic brain injury by inhibiting autophagy via increasing IL-10 production and blocking the AMPK/mTOR signaling pathway in rats.Metabolic brain disease · 2023Article
- Supplementary Pharmacotherapy for the Behavioral Abnormalities Caused by Stressors in Humans, Focused on Post-Traumatic Stress Disorder (PTSD).Journal of clinical medicine · 2023Article
- DCC/netrin-1 regulates cell death in oligodendrocytes after brain injury.Cell death and differentiation · 2023Article
- Formulating treatment of major psychiatric disorders: algorithm targets the dominantly affected brain cell-types.Discover mental health · 2023Review
- Advances in Traumatic Brain Injury Biomarkers.Cureus · 2022Review
- Minocycline improves the functional recovery after traumatic brain injury via inhibition of aquaporin-4.International journal of biological sciences · 2022Article
- Barcoded viral tracing of single-cell interactions in central nervous system inflammation.Science (New York, N.Y.) · 2021Article
- Irisin Rescues Blood-Brain Barrier Permeability following Traumatic Brain Injury and Contributes to the Neuroprotection of Exercise in Traumatic Brain Injury.Oxidative medicine and cellular longevity · 2021Article
- Ephs and Ephrins in Adult Endothelial Biology.International journal of molecular sciences · 2020Review
- Mechanisms of Blood-Brain Barrier Dysfunction in Traumatic Brain Injury.International journal of molecular sciences · 2020Review
- EphB3 interacts with initiator caspases and FHL-2 to activate dependence receptor cell death in oligodendrocytes after brain injury.Brain communications · 2020Article
- Angiopoietin/Tie2 Axis Regulates the Age-at-Injury Cerebrovascular Response to Traumatic Brain Injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
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Authors and funding
3 authors.
Funding
Abstract
Damage to the cerebrovascular network is a major contributor to dysfunction in patients suffering from traumatic brain injury (TBI). Vessels are composed of lumen-forming endothelial cells that associate closely with both glial and neuronal units to establish a functional blood-brain barrier (BBB). Under normal physiological conditions, these vascular units play important roles in central nervous system (CNS) homeostasis by delivering oxygen and nutrients while filtering out molecules and cells that could be harmful; however, after TBI this system is disrupted. Here, we describe a novel role for a class of receptors, called dependence receptors, in regulating vessel stability and BBB integrity after CCI injury in mice. Specifically, we identified that EphB3 receptors function as a pro-apoptotic dependence receptor in endothelial cells (ECs) that contributes to increased BBB damage after CCI injury. In the absence of EphB3, we observed increased endothelial cell survival, reduced BBB permeability and enhanced interactions of astrocyte-EC membranes. Interestingly, the brain's response to CCI injury is to reduce EphB3 levels and its ligand ephrinB3; however, the degree and timing of those reductions limit the protective response of the CNS. We conclude that EphB3 is a negative regulator of cell survival and BBB integrity that undermine tissue repair, and represents a protective therapeutic target for TBI patients.
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