ArticleJournal of neurotrauma2018
Intranasally Delivered Wnt3a Improves Functional Recovery after Traumatic Brain Injury by Modulating Autophagic, Apoptotic, and Regenerative Pathways in the Mouse Brain.
Article in Journal of neurotrauma, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 50 citations in OpenAlex.
- Integrated Necroptosis Within Programmed Cell Death in Traumatic Brain Injury.Molecular neurobiology · 2026Review
- Roles and regulatory mechanisms of autophagy in the pathology of spinal cord injury.Burns & trauma · 2026Review
- The Nasal-Brain Drug Delivery Route: Mechanisms and Applications to Central Nervous System Diseases.MedComm · 2025Review
- Blood-brain barrier disruption: a pervasive driver and mechanistic link between traumatic brain injury and Alzheimer's disease.Translational neurodegeneration · 2025Review
- Wnt/β-catenin Signaling in Central Nervous System Regeneration.Advances in experimental medicine and biology · 2025Review
- Transforming growth factor-β1 protects mechanically injured cortical murine neurons by reducing trauma-induced autophagy and apoptosis.Frontiers in cellular neuroscience · 2024Article
- Neuroprotective Effect of Hydrogen Sulfide Subchronic Treatment Against TBI-Induced Ferroptosis and Cognitive Deficits Mediated Through Wnt Signaling Pathway.Cellular and molecular neurobiology · 2023Article
- Neuroprotective potential of intranasally delivered L-myc immortalized human neural stem cells in female rats after a controlled cortical impact injury.Scientific reports · 2023Article
- High-fat diet feeding triggers a regenerative response in the adult zebrafish brain.Molecular neurobiology · 2023Article
- Targeting autophagy process in center nervous trauma.Frontiers in neuroscience · 2023Review
- The Role of Hydrogen Sulfide Targeting Autophagy in the Pathological Processes of the Nervous System.Metabolites · 2022Review
- Functionalized 3D-Printed ST2/Gelatin Methacryloyl/Polcaprolactone Scaffolds for Enhancing Bone Regeneration with Vascularization.International journal of molecular sciences · 2022Article
- Simvastatin rescues memory and granule cell maturation through the Wnt/β-catenin signaling pathway in a mouse model of Alzheimer's disease.Cell death & disease · 2022Article
- The role of regulatory necrosis in traumatic brain injury.Frontiers in molecular neuroscience · 2022Review
- Mitophagy in neurological disorders.Journal of neuroinflammation · 2021Review
- Human platelet lysate biotherapy for traumatic brain injury: preclinical assessment.Brain : a journal of neurology · 2021Article
- Review
- Microenvironmental Variations After Blood-Brain Barrier Breakdown in Traumatic Brain Injury.Frontiers in molecular neuroscience · 2021Review
- Novel Synthetic and Natural Therapies for Traumatic Brain Injury.Current neuropharmacology · 2021Review
- Elevated Dkk1 Mediates Downregulation of the Canonical Wnt Pathway and Lysosomal Loss in an iPSC Model of Neuronopathic Gaucher Disease.Biomolecules · 2020Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Traumatic brain injury (TBI) is a prevalent disorder, but no effective therapies currently exist. An underlying pathophysiology of TBI includes the pathological elevation of autophagy. β-Catenin, a downstream mediator of the canonical Wnt pathway, is a repressor of autophagy. The Wnt/β-catenin pathway plays a crucial role in cell proliferation and neuronal plasticity/repair in the adult brain. We hypothesized that activation of this pathway could promote neuroprotection and neural regeneration following TBI. In the controlled cortical impact (CCI) model of TBI in C57BL/6 mice (total n = 160), we examined intranasal application of recombinant Wnt3a (2 μg/kg) in a short-term (1 dose/day for 2 days) and long-term (1 dose/day for 7 days) regimen. Immunohistochemistry was performed at 1 to 14 days post-TBI to assess cell death and neurovascular regeneration. Western blotting measured canonical Wnt3a activity, expression of growth factors, and cell death markers. Longitudinal behavior assays evaluated functional recovery. In short-term experiments, Wnt3a treatment with a 60-min delay post-TBI suppressed TBI-induced autophagic activity in neurons (44.3 ± 6.98 and 4.25 ± 2.53 LC3+/NeuN+ double positive cells in TBI+Saline and TBI+Wnt3a mice, respectively; p < 0.0001, n = 5/group), reduced autophagic markers light chain 3 (LC3)-II and Beclin-1, as well as injury markers caspase-3 and matrix metalloproteinase 9 (MMP-9). The Wnt3a treatment reduced cell death and contusion volume (0.72 ± 0.07 mm
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