ArticleNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2021
Activation of Neurogenesis in Multipotent Stem Cells Cultured In Vitro and in the Spinal Cord Tissue After Severe Injury by Inhibition of Glycogen Synthase Kinase-3.
Article in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 21 citations in OpenAlex.
- The Canonical Wnt Surrogate Agonist scFv-Dkk1c Ameliorates Spinal Cord Injury in Rats.Molecular neurobiology · 2026Article
- Harnessing Endogenous Neural Stem Cells: A New Frontier in Spinal Cord Injury Repair.Neurochemical research · 2026Review
- Diversity, Functional Complexity, and Translational Potential of Glial Cells in the Central Nervous System.International journal of molecular sciences · 2025Review
- The Osteocyte with SB216763-Activated Canonical Wnt Signaling Constructs a Multifunctional 4D Intelligent Osteogenic Module.Biomolecules · 2024Article
- Effect of Electroacupuncture Stimulation on Proliferation and Differentiation of Endogenous Neural Stem Cells in Rats with Spinal Cord Injury.Molecular neurobiology · 2024Article
- Advancements in neuroregenerative and neuroprotective therapies for traumatic spinal cord injury.Frontiers in neuroscience · 2024Review
- Function of GSK‑3 signaling in spinal cord injury (Review).Experimental and therapeutic medicine · 2023Review
- The activation of dormant ependymal cells following spinal cord injury.Stem cell research & therapy · 2023Review
- miR-199a-5p from bone marrow mesenchymal stem cell exosomes promotes the proliferation of neural stem cells by targeting GSK-3β.Acta biochimica et biophysica Sinica · 2023Article
- Ependyma in Neurodegenerative Diseases, Radiation-Induced Brain Injury and as a Therapeutic Target for Neurotrophic Factors.Biomolecules · 2023Review
- Synthesis and biological evaluation of thieno[3,2-Journal of enzyme inhibition and medicinal chemistry · 2022Article
- Fish Hydrolysate Supplementation Prevents Stress-Induced Dysregulation of Hippocampal Proteins Relative to Mitochondrial Metabolism and the Neuronal Network in Mice.Foods (Basel, Switzerland) · 2022Article
- Neurogenesis as a Tool for Spinal Cord Injury.International journal of molecular sciences · 2022Review
- Exosomes Derived From Mesenchymal Stem Cells: Novel Effects in the Treatment of Ischemic Stroke.Frontiers in neuroscience · 2022Review
- Cell transplantation to repair the injured spinal cord.International review of neurobiology · 2022Article
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Authors and funding
12 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The inhibition of glycogen synthase kinase-3 (GSK-3) can induce neurogenesis, and the associated activation of Wnt/β-catenin signaling via GSK-3 inhibition may represent a means to promote motor function recovery following spinal cord injury (SCI) via increased astrocyte migration, reduced astrocyte apoptosis, and enhanced axonal growth. Herein, we assessed the effects of GSK-3 inhibition in vitro on the neurogenesis of ependymal stem/progenitor cells (epSPCs) resident in the mouse spinal cord and of human embryonic stem cell-derived neural progenitors (hESC-NPs) and human-induced pluripotent stem cell-derived neural progenitors (hiPSC-NPs) and in vivo on spinal cord tissue regeneration and motor activity after SCI. We report that the treatment of epSPCs and human pluripotent stem cell-derived neural progenitors (hPSC-NPs) with the GSK-3 inhibitor Ro3303544 activates β-catenin signaling and increases the expression of the bIII-tubulin neuronal marker; furthermore, the differentiation of Ro3303544-treated cells prompted an increase in the number of terminally differentiated neurons. Administration of a water-soluble, bioavailable form of this GSK-3 inhibitor (Ro3303544-Cl) in a severe SCI mouse model revealed the increased expression of bIII-tubulin in the injury epicenter. Treatment with Ro3303544-Cl increased survival of mature neuron types from the propriospinal tract (vGlut1, Parv) and raphe tract (5-HT), protein kinase C gamma-positive neurons, and GABAergic interneurons (GAD65/67) above the injury epicenter. Moreover, we observed higher numbers of newly born BrdU/DCX-positive neurons in Ro3303544-Cl-treated animal tissues, a reduced area delimited by astrocyte scar borders, and improved motor function. Based on this study, we believe that treating animals with epSPCs or hPSC-NPs in combination with Ro3303544-Cl deserves further investigation towards the development of a possible therapeutic strategy for SCI.
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