ArticleASN neuro2014
Comparison of cortical and white matter traumatic brain injury models reveals differential effects in the subventricular zone and divergent Sonic hedgehog signaling pathways in neuroblasts and oligodendrocyte progenitors.
Article in ASN neuro, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
28 citing papers in PubMed, 46 citations in OpenAlex.
- Article
- The role of Smo-Shh/Gli signaling activation in the prevention of neurological and ageing disorders.Biogerontology · 2023Review
- Review
- Acute axon damage and demyelination are mitigated by 4-aminopyridine (4-AP) therapy after experimental traumatic brain injury.Acta neuropathologica communications · 2022Article
- An implantable human stem cell-derived tissue-engineered rostral migratory stream for directed neuronal replacement.Communications biology · 2021Article
- Review
- Sonic hedgehog signaling in astrocytes.Cellular and molecular life sciences : CMLS · 2021Review
- Repetitive Blast Exposure Produces White Matter Axon Damage without Subsequent Myelin Remodeling:Neurotrauma reports · 2021Article
- Sonic Hedgehog Signaling Promotes Peri-Lesion Cell Proliferation and Functional Improvement after Cortical Contusion Injury.Neurotrauma reports · 2021Article
- Activation of the Hedgehog Pathway Promotes Recovery of Neurological Function After Traumatic Brain Injury by Protecting the Neurovascular Unit.Translational stroke research · 2020Article
- Olfactory Dysfunction in Traumatic Brain Injury: the Role of Neurogenesis.Current allergy and asthma reports · 2020Review
- Diffuse Axonal Injury in the Rat Brain: Axonal Injury and Oligodendrocyte Activity Following Rotational Injury.Brain sciences · 2020Article
- Tissue Engineering and Biomaterial Strategies to Elicit Endogenous Neuronal Replacement in the Brain.Frontiers in neurology · 2020Review
- Purmorphamine Attenuates Neuro-Inflammation and Synaptic Impairments After Hypoxic-Ischemic Injury in Neonatal Mice via Shh Signaling.Frontiers in pharmacology · 2020Article
- Neuroprotective Effects of the Sonic Hedgehog Signaling Pathway in Ischemic Injury through Promotion of Synaptic and Neuronal Health.Neural plasticity · 2020Article
- Sonic hedgehog signaling is negatively regulated in reactive astrocytes after forebrain stab injury.Scientific reports · 2019Article
- FAM19A5 Expression During Embryogenesis and in the Adult Traumatic Brain ofFrontiers in neuroscience · 2019Article
- Targeting Smoothened as a New Frontier in the Functional Recovery of Central Nervous System Demyelinating Pathologies.International journal of molecular sciences · 2018Review
- The Elegance of Sonic Hedgehog: Emerging Novel Functions for a Classic Morphogen.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Review
- Experimental Traumatic Brain Injury Identifies Distinct Early and Late Phase Axonal Conduction Deficits of White Matter Pathophysiology, and Reveals Intervening Recovery.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The regenerative capacity of the central nervous system must be optimized to promote repair following traumatic brain injury (TBI) and may differ with the site and form of damage. Sonic hedgehog (Shh) maintains neural stem cells and promotes oligodendrogenesis. We examined whether Shh signaling contributes to neuroblast (doublecortin) or oligodendrocyte progenitor (neural/glial antigen 2 [NG2]) responses in two distinct TBI models. Shh-responsive cells were heritably labeled in vivo using Gli1-CreER(T2);R26-YFP bitransgenic mice with tamoxifen administration on Days 2 and 3 post-TBI. Injury to the cerebral cortex was produced with mild controlled cortical impact. Yellow fluorescent protein (YFP) cells decreased in cortical lesions. Total YFP cells increased in the subventricular zone (SVZ), indicating Shh pathway activation in SVZ cells, including doublecortin-labeled neuroblasts. The alternate TBI model produced traumatic axonal injury in the corpus callosum. YFP cells decreased within the SVZ and were rarely double labeled as NG2 progenitors. NG2 progenitors increased in the cortex, with a similar pattern in the corpus callosum. To further test the potential of NG2 progenitors to respond through Shh signaling, Smoothened agonist was microinjected into the corpus callosum to activate Shh signaling. YFP cells and NG2 progenitors increased in the SVZ but were not double labeled. This result indicates that either direct Smoothened activation in NG2 progenitors does not signal through Gli1 or that Smoothened agonist acts indirectly to increase NG2 progenitors. Therefore, in all conditions, neuroblasts exhibited differential Shh pathway utilization compared with oligodendrocyte progenitors. Notably, cortical versus white matter damage from TBI produced opposite responses of Shh-activated cells within the SVZ.
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