ArticleASN neuro2009
Brain injury expands the numbers of neural stem cells and progenitors in the SVZ by enhancing their responsiveness to EGF.
Article in ASN neuro, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 61 citations in OpenAlex.
- Application of injectable hydrogels in the central and peripheral nervous system as a unique and flexible platform for neural tissue repair.Materials today. Bio · 2025Review
- High spatial resolution gene expression profiling and characterization of neuroblasts migrating in the peri-injured cortex using photo-isolation chemistry.Frontiers in neuroscience · 2024Article
- Can the administration of platelet lysates to the brain help treat neurological disorders?Cellular and molecular life sciences : CMLS · 2022Review
- Subventricular zone adult mouse neural stem cells require insulin receptor for self-renewal.Stem cell reports · 2022Article
- Stem Cell Therapy for Pediatric Traumatic Brain Injury.Frontiers in neurology · 2020Review
- Dentate Gyrus Proliferative Responses After Traumatic Brain Injury and Binge Alcohol in Adult Rats.Neuroscience insights · 2020Article
- Intrinsic Mechanisms Regulating Neuronal Migration in the Postnatal Brain.Frontiers in cellular neuroscience · 2020Review
- Subventricular zone neural precursor cell responses after traumatic brain injury and binge alcohol in male rats.Journal of neuroscience research · 2019Article
- Astragaloside VI Promotes Neural Stem Cell Proliferation and Enhances Neurological Function Recovery in Transient Cerebral Ischemic Injury via Activating EGFR/MAPK Signaling Cascades.Molecular neurobiology · 2019Article
- The Role of SVZ Stem Cells in Glioblastoma.Cancers · 2019Review
- Ginkgolide B promotes the proliferation and differentiation of neural stem cells following cerebral ischemia/reperfusion injury, bothNeural regeneration research · 2018Article
- Hemopexin is required for adult neurogenesis in the subventricular zone/olfactory bulb pathway.Cell death & disease · 2018Article
- Pediatric brain repair from endogenous neural stem cells of the subventricular zone.Pediatric research · 2018Review
- Olig1 is required for noggin-induced neonatal myelin repair.Annals of neurology · 2017Article
- Unmasking the responses of the stem cells and progenitors in the subventricular zone after neonatal and pediatric brain injuries.Neural regeneration research · 2016Review
- Subarachnoid Hemorrhage Promotes Proliferation, Differentiation, and Migration of Neural Stem Cells via BDNF Upregulation.PloS one · 2016Article
- Mechanisms of mouse neural precursor expansion after neonatal hypoxia-ischemia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Endogenous repair signaling after brain injury and complementary bioengineering approaches to enhance neural regeneration.Biomarker insights · 2015Review
- Traumatic brain injury reveals novel cell lineage relationships within the subventricular zone.Stem cell research · 2014Article
- Ribosomal S6 kinase regulates ischemia-induced progenitor cell proliferation in the adult mouse hippocampus.Experimental neurology · 2014Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
There is an increase in the numbers of neural precursors in the SVZ (subventricular zone) after moderate ischaemic injuries, but the extent of stem cell expansion and the resultant cell regeneration is modest. Therefore our studies have focused on understanding the signals that regulate these processes towards achieving a more robust amplification of the stem/progenitor cell pool. The goal of the present study was to evaluate the role of the EGFR [EGF (epidermal growth factor) receptor] in the regenerative response of the neonatal SVZ to hypoxic/ischaemic injury. We show that injury recruits quiescent cells in the SVZ to proliferate, that they divide more rapidly and that there is increased EGFR expression on both putative stem cells and progenitors. With the amplification of the precursors in the SVZ after injury there is enhanced sensitivity to EGF, but not to FGF (fibroblast growth factor)-2. EGF-dependent SVZ precursor expansion, as measured using the neurosphere assay, is lost when the EGFR is pharmacologically inhibited, and forced expression of a constitutively active EGFR is sufficient to recapitulate the exaggerated proliferation of the neural stem/progenitors that is induced by hypoxic/ischaemic brain injury. Cumulatively, our results reveal that increased EGFR signalling precedes that increase in the abundance of the putative neural stem cells and our studies implicate the EGFR as a key regulator of the expansion of SVZ precursors in response to brain injury. Thus modulating EGFR signalling represents a potential target for therapies to enhance brain repair from endogenous neural precursors following hypoxic/ischaemic and other brain injuries.
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Registered trials
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.