ArticleStem cells (Dayton, Ohio)2010
EphB3 limits the expansion of neural progenitor cells in the subventricular zone by regulating p53 during homeostasis and following traumatic brain injury.
Article in Stem cells (Dayton, Ohio), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 82 citations in OpenAlex.
- Master regulators of neurogenesis: the dynamic roles of Ephrin receptors across diverse cellular niches.Translational psychiatry · 2024Review
- DCC/netrin-1 regulates cell death in oligodendrocytes after brain injury.Cell death and differentiation · 2023Article
- Will Cannabigerol Trigger Neuroregeneration after a Spinal Cord Injury? An In Vitro Answer from NSC-34 Scratch-Injured Cells Transcriptome.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Type I Interferon Response Is Mediated by NLRX1-cGAS-STING Signaling in Brain Injury.Frontiers in molecular neuroscience · 2022Article
- Abrogation of atypical neurogenesis and vascular-derived EphA4 prevents repeated mild TBI-induced learning and memory impairments.Scientific reports · 2020Article
- Peripheral loss of EphA4 ameliorates TBI-induced neuroinflammation and tissue damage.Journal of neuroinflammation · 2019Article
- Divergent age-dependent peripheral immune transcriptomic profile following traumatic brain injury.Scientific reports · 2019Article
- 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
- Roles of Eph/ephrin bidirectional signaling during injury and recovery of the central nervous system.Neural regeneration research · 2018Review
- Roles of Eph/ephrin bidirectional signaling in central nervous system injury and recovery.Experimental and therapeutic medicine · 2018Article
- EphB3 signaling induces cortical endothelial cell death and disrupts the blood-brain barrier after traumatic brain injury.Cell death & disease · 2018Article
- Transcriptional Profiling of Ligand Expression in Cell Specific Populations of the Adult Mouse Forebrain That Regulates Neurogenesis.Frontiers in neuroscience · 2018Article
- Loss of NLRX1 Exacerbates Neural Tissue Damage and NF-κB Signaling following Brain Injury.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Modulation of gap junction-associated Cx43 in neural stem/progenitor cells following traumatic brain injury.Brain research bulletin · 2017Article
- EphA4 Regulates Neuroblast and Astrocyte Organization in a Neurogenic Niche.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- EphrinB3 restricts endogenous neural stem cell migration after traumatic brain injury.Stem cell research · 2016Article
- EphB3 signaling propagates synaptic dysfunction in the traumatic injured brain.Neurobiology of disease · 2016Article
- A Compact Blast-Induced Traumatic Brain Injury Model in Mice.Journal of neuropathology and experimental neurology · 2016Article
- Endothelial-Specific EphA4 Negatively Regulates Native Pial Collateral Formation and Re-Perfusion following Hindlimb Ischemia.PloS one · 2016Article
- Traumatic Brain Injury Activation of the Adult Subventricular Zone Neurogenic Niche.Frontiers in neuroscience · 2016Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Ephrins and Eph receptor(s) have recently been implicated in regulating neurogenesis in the adult subventricular zone (SVZ) and rostral migratory stream. Here, we examined the role of ephrinB3-EphB3 signaling in mediating the SVZ response to traumatic brain injury (TBI). Analysis of EphB3 expression showed colocalization with glial fibrillary acidic protein-positive neural stem progenitor cells (NSPCs) and doublecortin-positive neuroblasts, whereas ephrinB3 was expressed outside the neurogenic region. TBI resulted in a significant reduction in EphB3 expression, which coincided with enhanced NSPC survival and proliferation at 3 and 7 days postinjury. Analysis of mice lacking either ephrinB3 (ephrinB3(-/-)) or EphB3 (EphB3(-/-)) showed a significant increase in bromodeoxyuridine (BrdU) incorporation and Ki67 immunoreactivity in the SVZ. Interestingly, cell death was dissimilar between knockout mice, where cell death was reduced in EphB3(-/-) but increased in ephrinB3(-/-) mice. Lateral ventricle infusion of soluble preclustered ephrinB3-Fc reversed the proliferative and cell death defects in ephrinB3(-/-) but not EphB3(-/-) mice and prevented TBI-induced proliferation in wild-type NSPCs. Coincidently, tumor suppressor p53 expression was increased following EphB3 stimulation and is reduced in the absence of either EphB3 or ephrinB3. Furthermore, pharmacological inhibition and siRNA knockdown of p53-attenuated ephrinB3-Fc-mediated growth suppression while having no effect on cell death in cultured NSPCs. These data demonstrate that EphB3 signaling suppresses NSPC proliferation in a p53-dependent manner, induces cell death in the absence of ligand stimulation and is transiently reduced in the SVZ to initiate the expansion and survival of endogenous adult NSPCs following TBI.
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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.