PUBLICATION
            Semaphorin4D promotes axon regrowth and swimming ability during recovery following zebrafish spinal cord injury
- Authors
 - Peng, S.X., Yao, L., Cui, C., Zhao, H.D., Liu, C.J., Li, Y.H., Wang, L.F., Huang, S.B., Shen, Y.Q.
 - ID
 - ZDB-PUB-170330-21
 - Date
 - 2017
 - Source
 - Neuroscience 351: 36-46 (Journal)
 - Registered Authors
 - Keywords
 - Axon regeneration, Microglia, Semaphorin4D, Spinal cord injury, Zebrafish
 - MeSH Terms
 - 
    
        
        
            
                
- Spinal Cord Injuries/genetics
 - Spinal Cord Injuries/metabolism*
 - Spinal Cord Injuries/physiopathology*
 - Zebrafish Proteins/genetics
 - Zebrafish Proteins/metabolism*
 - Axons/metabolism*
 - Recovery of Function/physiology*
 - Motor Neurons/metabolism
 - Disease Models, Animal
 - Zebrafish
 - Locomotion/physiology*
 - Spinal Cord/metabolism
 - Smad Proteins/genetics
 - Smad Proteins/metabolism*
 - Animals
 - Spinal Cord Regeneration/physiology*
 - Swimming
 
 - PubMed
 - 28347780 Full text @ Neuroscience
 
            Citation
        
        
            Peng, S.X., Yao, L., Cui, C., Zhao, H.D., Liu, C.J., Li, Y.H., Wang, L.F., Huang, S.B., Shen, Y.Q. (2017) Semaphorin4D promotes axon regrowth and swimming ability during recovery following zebrafish spinal cord injury. Neuroscience. 351:36-46.
        
    
                
                    
                        Abstract
                    
                    
                
                
            
        
        
    
        
            
            
 
    
    
        
    
    
    
        
                Semaphorins comprise a family of proteins involved in axon guidance during development. Semaphorin4D (Sema4D) has both neuroregenerative and neurorepressive functions, being able to stimulate both axonal outgrowth and growth cone collapse during development, and therefore could play an important role in neurological recovery from traumatic injury. Here, we used a zebrafish spinal cord transection model to study the role of Sema4D in a system capable of neuroregeneration. Real-time qPCR and in situ hybridization showed upregulated Sema4D expression in the acute response phase (within 3 days post SCI), and downregulated levels in the chronic response phase (11-21 days after SCI). Double-immunostaining for Sema4D and either Islet-1 (motoneuron marker) or Iba-1 (microglial marker) showed that microglia surrounded Sema4D-positive motoneurons along the central canal at 4 hours post injury (hpi) and 12 hpi. Following administration of Sema4D morpholino to transected zebrafish, double-immunostaining showed that Sema4D-positive motoneurons surrounded by microglia decreased at 7 days and 11 days compared with standard control morpholino. Anterograde and retrograde tracing indicate that Sema4D participates in axon regeneration in the spinal cord following SCI in the zebrafish. Swim tracking shows that morpholino-mediated inhibition of Sema4D retarded the recovery of swimming function when compared to standard control morpholino. The combined results indicate that Sema4D expression in motoneurons enhances locomotor recovery and axon regeneration, possibly by regulating microglia function, after spinal cord injury in adult zebrafish.
            
    
        
        
    
    
    
                
                    
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