ArticleNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2012
C3 peptide promotes axonal regeneration and functional motor recovery after peripheral nerve injury.
Article in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Advancement of Electrospun Nerve Conduit for Peripheral Nerve Regeneration: A Systematic Review (2016-2021).International journal of nanomedicine · 2022Pooled it
- Peptide-Incorporated Biomaterials Promote Regeneration of Peripheral Nerve Injuries.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Engineered bio-functional material-based nerve guide conduits for optic nerve regeneration: a view from the cellular perspective, challenges and the future outlook.Regenerative biomaterials · 2025Review
- Emerging role of extracellular vesicles and exogenous stimuli in molecular mechanisms of peripheral nerve regeneration.Frontiers in cellular neuroscience · 2024Review
- Discovery of novel immunotherapeutic drug candidates for sciatic nerve injury using bioinformatic analysis and experimental verification.Frontiers in pharmacology · 2022Article
- Gene correlation network analysis to identify regulatory factors in sciatic nerve injury.Journal of orthopaedic surgery and research · 2021Article
- Potentiation of Brain-Derived Neurotrophic Factor-Induced Protection of Spiral Ganglion Neurons by C3 Exoenzyme/Rho Inhibitor.Frontiers in cellular neuroscience · 2021Article
- Review
- Extracellular Vesicles Derived From Olfactory Ensheathing Cells Promote Peripheral Nerve Regeneration in Rats.Frontiers in cellular neuroscience · 2019Article
- Traumatic Brain Injuries: Pathophysiology and Potential Therapeutic Targets.Frontiers in cellular neuroscience · 2019Review
- MotomiRs: miRNAs in Motor Neuron Function and Disease.Frontiers in molecular neuroscience · 2017Review
- Cyclic AMP signaling: a molecular determinant of peripheral nerve regeneration.BioMed research international · 2014Review
- Vimentin mediates uptake of C3 exoenzyme.PloS one · 2014Article
- Rho-independent stimulation of axon outgrowth and activation of the ERK and Akt signaling pathways by C3 transferase in sensory neurons.Frontiers in cellular neuroscience · 2012Article
- Cell Entry of C3 Exoenzyme from Clostridium botulinum.Current topics in microbiology and immunologyReview
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9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Peripheral nerve injuries are frequently seen in trauma patients and due to delayed nerve repair, lifelong disabilities often follow this type of injury. Innovative therapies are needed to facilitate and expedite peripheral nerve regeneration. The purpose of this study was to determine the effects of a 1-time topical application of a 26-amino-acid fragment (C3(156-181)), derived from the Clostridium botulinum C3-exoenzyme, on peripheral nerve regeneration in 2 models of nerve injury and repair in adult rats. After sciatic nerve crush, different dosages of C3(156-181) dissolved in buffer or reference solutions (nerve growth factor or C3(bot)-wild-type protein) or vehicle-only were injected through an epineurial opening into the lesion sites. After 10-mm nerve autotransplantation, either 8.0 nmol/kg C3(156-181) or vehicle were injected into the proximal and distal suture sites. For a period of 3 to 10 postoperative weeks, C3(156-181)-treated animals showed a faster motor recovery than control animals. After crush injury, axonal outgrowth and elongation were activated and consequently resulted in faster motor recovery. The nerve autotransplantation model further elucidated that C3(156-181) treatment accounts for better axonal elongation into motor targets and reduced axonal sprouting, which are followed by enhanced axonal maturation and better axonal functionality. The effects of C3(156-181) are likely caused by a nonenzymatic down-regulation of active RhoA. Our results indicate the potential of C3(156-181) as a therapeutic agent for the topical treatment of peripheral nerve repair sites.
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