PUBLICATION
            Prolonged neutrophil retention in the wound impairs zebrafish heart regeneration after cryoinjury
- Authors
- Xu, S., Xie, F., Tian, L., Manno, S.H., Manno, F.A.M., Cheng, S.H.
- ID
- ZDB-PUB-190919-3
- Date
- 2019
- Source
- Fish & shellfish immunology 94: 447-454 (Journal)
- Registered Authors
- Cheng, Shuk Han
- Keywords
- AKT/mTOR, Cryoinjury, Heart regeneration, Neutrophil, Retention, Reverse migration
- MeSH Terms
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                - Animals
- Freezing/adverse effects*
- Neutrophils/immunology
- Heart/physiology*
- Cryopreservation/veterinary
- Heart Injuries/etiology
- Heart Injuries/physiopathology
- Regeneration*
- Zebrafish/physiology*
- Signal Transduction/physiology*
 
- PubMed
- 31526847 Full text @ Fish Shellfish Immunol.
            Citation
        
        
            Xu, S., Xie, F., Tian, L., Manno, S.H., Manno, F.A.M., Cheng, S.H. (2019) Prolonged neutrophil retention in the wound impairs zebrafish heart regeneration after cryoinjury. Fish & shellfish immunology. 94:447-454.
        
    
                
                    
                        Abstract
                    
                    
                
                
            
        
        
    
        
            
            
 
    
    
        
    
    
    
        
                Neutrophils are the first line defenders in the innate immune response, and rapidly migrate to an infected or injured area. Recently, bidirectional migration of neutrophils to the wound and the corresponding functions have become popular research pursuits. In zebrafish larvae, CXCR1/CXCL8 is the predominant chemoattractant pathway to recruit neutrophil to wound, while CXCR2/CXCL8 pathway mediate neutrophil dispersal in wound after injury. Here, we found that both CXCR1/CXCL8 and LTB4/BLT1 signals are activated in zebrafish heart after cryoinjury. And with a CXCR1/2 selective inhibitor (SB225002) treatment, the recruitment of neutrophils was not affected, but reverse migration of neutrophils was inhibited after cryoinjury of heart. We suggested that the neutrophil recruitment to cryoinjured area might be mediated by LTB4/BLT1 signals at the presence of SB225002. Therefore, SB225002 treatment resulted more accumulation and long retention of neutrophils in the injured heart. The long retention of neutrophils in the wound promoted revascularization in the injured heart; however, the AKT/mTOR pathway was inhibited and the regeneration was impaired. Our findings suggest that retention of neutrophils is a well-orchestrated process and might regulate regeneration by the AKT/mTOR pathway.
            
    
        
        
    
    
    
                
                    
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