PUBLICATION
            P130Cas/bcar1 mediates zebrafish caudal vein plexus angiogenesis
- Authors
- Wisniewski, L., French, V., Lockwood, N., Valdivia, L.E., Frankel, P.
- ID
- ZDB-PUB-201002-160
- Date
- 2020
- Source
- Scientific Reports 10: 15589 (Journal)
- Registered Authors
- Valdivia, Leonardo
- Keywords
- none
- MeSH Terms
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                - Neovascularization, Physiologic*
- Embryo, Nonmammalian/cytology
- Embryo, Nonmammalian/physiology*
- Veins/embryology
- Veins/physiology*
- Animals
- Animals, Genetically Modified/embryology
- Animals, Genetically Modified/physiology*
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism*
- Zebrafish/embryology
- Zebrafish/physiology*
- Bone Morphogenetic Protein 2/genetics
- Bone Morphogenetic Protein 2/metabolism
 
- PubMed
- 32973180 Full text @ Sci. Rep.
            Citation
        
        
            Wisniewski, L., French, V., Lockwood, N., Valdivia, L.E., Frankel, P. (2020) P130Cas/bcar1 mediates zebrafish caudal vein plexus angiogenesis. Scientific Reports. 10:15589.
        
    
                
                    
                        Abstract
                    
                    
                
                
            
        
        
    
        
            
            
 
    
    
        
    
    
    
        
                P130CAS/BCAR1 belongs to the CAS family of adaptor proteins, with important regulatory roles in cell migration, cell cycle control, and apoptosis. Previously, we and others showed that P130CAS mediates VEGF-A and PDGF signalling in vitro, but its cardiovascular function in vivo remains relatively unexplored. We characterise here a novel deletion model of P130CAS in zebrafish. Using in vivo microscopy and transgenic vascular reporters, we observed that while bcar1-/- zebrafish showed no arterial angiogenic or heart defects during development, they strikingly failed to form the caudal vein plexus (CVP). Endothelial cells (ECs) within the CVP of bcar1-/- embryos produced fewer filopodial structures and did not detach efficiently from neighbouring cells, resulting in a significant reduction in ventral extension and overall CVP area. Mechanistically, we show that P130Cas mediates Bmp2b-induced ectopic angiogenic sprouting of ECs in the developing embryo and provide pharmacological evidence for a role of Src family kinases in CVP development.
            
    
        
        
    
    
    
                
                    
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