ArticleMolecular neurobiology2018
Chondroitin Sulfate Impairs Neural Stem Cell Migration Through ROCK Activation.
Article in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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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
29 citing papers in PubMed, 67 citations in OpenAlex.
- Innovative Biomaterials for Modulating Neuroinflammation and Promoting Repair After Traumatic Brain Injury.Pharmaceutics · 2026Review
- Mechanobiology of hippocampal neurogenesis: directing neural stem cell fate through physical cues.Frontiers in molecular neuroscience · 2026Review
- A Review of the Potential Use of Antioxidants in Spinal Cord Injuries.Antioxidants (Basel, Switzerland) · 2025Review
- Pathophysiology of spinal cord injury and advanced therapeutic approaches.Molecular biology reports · 2025Review
- Proteoglycans and glycosaminoglycans: critical regulators in angiogenesis, vasculogenesis, and vascularized tissue engineering.Angiogenesis · 2025Review
- Recent Advances in Enzymes and Chemoenzymatic Synthesis of Tetrasaccharide Linkage Region of Proteoglycans.Chembiochem : a European journal of chemical biology · 2025Review
- Schwann Cells and Their Exosomes: Research Progress and Prospect in Spinal Cord Injury.Neural plasticity · 2025Review
- Diacylglycerol kinase γ facilitates the proliferation and migration of neural stem cells in the developing neural tube.Acta biochimica et biophysica Sinica · 2024Article
- Enhanced axon outgrowth of spinal motor neurons in co-culturing with dorsal root ganglions antagonizes the growth inhibitory environment.Regenerative therapy · 2024Article
- Chondroitin Sulfate Proteoglycans Revisited: Its Mechanism of Generation and Action for Spinal Cord Injury.Aging and disease · 2024Review
- Agomir-331 Suppresses Reactive Gliosis and Neuroinflammation after Traumatic Brain Injury.Cells · 2023Article
- Chromatin accessibility dynamics of neurogenic niche cells reveal defects in neural stem cell adhesion and migration during aging.Nature aging · 2023Article
- Molecular mediators of angiogenesis and neurogenesis after ischemic stroke.Reviews in the neurosciences · 2023Article
- Neural stem cells transplantation combined with ethyl stearate improve PD rats motor behavior by promoting NSCs migration and differentiation.CNS neuroscience & therapeutics · 2023Article
- The Impact of the Cellular Environment and Aging on Modeling Alzheimer's Disease in 3D Cell Culture Models.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Review
- Chemistry and Function of Glycosaminoglycans in the Nervous System.Advances in neurobiology · 2023Review
- Alpha-SNAP (M105I) mutation promotes neuronal differentiation of neural stem/progenitor cells through overactivation of AMPK.Frontiers in cell and developmental biology · 2023Article
- Characterization of Hyaluronidase 4 Involved in the Catabolism of Chondroitin Sulfate.Molecules (Basel, Switzerland) · 2022Article
- Inhibition of CSPG receptor PTPσ promotes migration of newly born neuroblasts, axonal sprouting, and recovery from stroke.Cell reports · 2022Article
- Microglia as hackers of the matrix: sculpting synapses and the extracellular space.Cellular & molecular immunology · 2021Review
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
Abstract
Brain injuries such as trauma and stroke lead to glial scar formation by reactive astrocytes which produce and secret axonal outgrowth inhibitors. Chondroitin sulfate proteoglycans (CSPG) constitute a well-known class of extracellular matrix molecules produced at the glial scar and cause growth cone collapse. The CSPG glycosaminoglycan side chains composed of chondroitin sulfate (CS) are responsible for its inhibitory activity on neurite outgrowth and are dependent on RhoA activation. Here, we hypothesize that CSPG also impairs neural stem cell migration inhibiting their penetration into an injury site. We show that DCX+ neuroblasts do not penetrate a CSPG-rich injured area probably due to Nogo receptor activation and RhoA/ROCK signaling pathway as we demonstrate in vitro with neural stem cells cultured as neurospheres and pull-down for RhoA. Furthermore, CS-impaired cell migration in vitro induced the formation of large mature adhesions and altered cell protrusion dynamics. ROCK inhibition restored migration in vitro as well as decreased adhesion size.
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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.