PUBLICATION
            Nuclear Receptor Subfamily 2 Group F Member 1a (nr2f1a) Is Required for Vascular Development in Zebrafish
- Authors
 - Wu, B.J., Chiu, C.C., Chen, C.L., Wang, W.D., Wang, J.H., Wen, Z.H., Liu, W., Chang, H.W., Wu, C.Y.
 - ID
 - ZDB-PUB-140827-3
 - Date
 - 2014
 - Source
 - PLoS One 9: e105939 (Journal)
 - Registered Authors
 - Wang, Wen-Der
 - Keywords
 - Embryos, Zebrafish, Morpholino, Angiogenesis, Notch signaling, Edema, Veins, Vertebrates
 - MeSH Terms
 - 
    
        
        
            
                
- Gene Expression
 - Zebrafish/physiology*
 - Amino Acid Sequence
 - Neovascularization, Physiologic*
 - Conserved Sequence
 - Zebrafish Proteins/physiology*
 - Animals
 - Endothelium, Vascular/growth & development
 - Endothelium, Vascular/metabolism
 - Molecular Sequence Data
 - DNA-Binding Proteins/physiology*
 - Gene Expression Regulation, Developmental
 - Transcription Factors/physiology*
 
 - PubMed
 - 25157918 Full text @ PLoS One
 
            Citation
        
        
            Wu, B.J., Chiu, C.C., Chen, C.L., Wang, W.D., Wang, J.H., Wen, Z.H., Liu, W., Chang, H.W., Wu, C.Y. (2014) Nuclear Receptor Subfamily 2 Group F Member 1a (nr2f1a) Is Required for Vascular Development in Zebrafish. PLoS One. 9:e105939.
        
    
                
                    
                        Abstract
                    
                    
                
                
            
        
        
    
        
            
            
 
    
    
        
    
    
    
        
                Genetic regulators and signaling pathways are important for the formation of blood vessels. Transcription factors controlling vein identity, intersegmental vessels (ISV) growth and caudal vein plexus (CVP) formation in zebrafish are little understood as yet. Here, we show the importance of the nuclear receptor subfamily member 1A (nr2f1a) in zebrafish vascular development. Amino acid sequence alignment and phylogenetic analysis of nr2f1a is highly conserved among the vertebrates. Our in situ hybridization results showed nr2f1a mRNA is expressed in the lateral plate mesoderm at 18 somite stage and in vessels at 24-30 hpf, suggesting its roles in vasculization. Consistent with this morpholino-based knockdown of nr2fla impaired ISV growth and failed to develop fenestrated vascular structure in CVP, suggesting that nr2f1a has important roles in controlling ISV and CVP growth. Consequently, nr2f1a morphants showed pericardial edema and circulation defects. We further demonstrated reduced ISV cells and decreased CVP endothelial cells sprouting in nr2f1a morphants, indicating the growth impairment of ISV and CVP is due to a decrease of cell proliferation and migration, but not results from cell death in endothelial cells after morpholino knockdown. To test molecular mechanisms and signals that are associated with nr2f1a, we examined the expression of vascular markers. We found that a loss of nr2f1a results in a decreased expression of vein/ISV specific markers, flt4, mrc1, vascular markers stabilin and ephrinb2. This indicates the regulatory role of nr2f1a in controlling vascular development. We further showed that nr2f1a likely interact with Notch signaling by examining nr2f1a expression in rbpsuh morphants and DAPT-treatment embryos. Together, we show nr2f1a plays a critical role for vascular development in zebrafish.
            
    
        
        
    
    
    
                
                    
                        Genes / Markers
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Expression
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Phenotype
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Mutations / Transgenics
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Human Disease / Model
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Sequence Targeting Reagents
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Fish
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Orthology
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Engineered Foreign Genes
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Mapping