Lorber, B.* ; Chew, D.J.* ; Hauck, S.M. ; Chong, R.S.* ; Fawcett, J.W.* ; Martin, K.R.*
     
 
    
        
Retinal glia promote dorsal root ganglion axon regeneration.
    
    
        
    
    
        
        PLoS ONE 10:e0115996 (2015)
    
    
    
		
		
			
				Axon regeneration in the adult central nervous system (CNS) is limited by several factors including a lack of neurotrophic support. Recent studies have shown that glia from the adult rat CNS, specifically retinal astrocytes and Müller glia, can promote regeneration of retinal ganglion cell axons. In the present study we investigated whether retinal glia also exert a growth promoting effect outside the visual system. We found that retinal glial conditioned medium significantly enhanced neurite growth and branching of adult rat dorsal root ganglion neurons (DRG) in culture. Furthermore, transplantation of retinal glia significantly enhanced regeneration of DRG axons past the dorsal root entry zone after root crush in adult rats. To identify the factors that mediate the growth promoting effects of retinal glia, mass spectrometric analysis of retinal glial conditioned medium was performed. Apolipoprotein E and secreted protein acidic and rich in cysteine (SPARC) were found to be present in high abundance, a finding further confirmed by western blotting. Inhibition of Apolipoprotein E and SPARC significantly reduced the neuritogenic effects of retinal glial conditioned medium on DRG in culture, suggesting that Apolipoprotein E and SPARC are the major mediators of this regenerative response.
			
			
				
			
		 
		
			
				
					
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        Publikationstyp
        Artikel: Journalartikel
    
 
    
        Dokumenttyp
        Wissenschaftlicher Artikel
    
 
    
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        Schlagwörter
        Receptor-related Protein-1; Apolipoprotein-e; Neurite Outgrowth; Mesangial Cells; Spinal-cord; In-vitro; Sparc; Survival; Lipoproteins; Osteonectin
    
 
    
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        englisch
    
 
    
        Veröffentlichungsjahr
        2015
    
 
    
        Prepublished im Jahr 
        
    
 
    
        HGF-Berichtsjahr
        2015
    
 
    
    
        ISSN (print) / ISBN
        1932-6203
    
 
    
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	    Band: 10,  
	    Heft: 3,  
	    Seiten: ,  
	    Artikelnummer: e0115996 
	    Supplement: ,  
	
    
 
  
        
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            Verlag
            Public Library of Science (PLoS)
        
 
        
            Verlagsort
            Lawrence, Kan.
        
 
	
        
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        Begutachtungsstatus
        Peer reviewed
    
 
     
    
        POF Topic(s)
        30203 - Molecular Targets and Therapies
    
 
    
        Forschungsfeld(er)
        Enabling and Novel Technologies
    
 
    
        PSP-Element(e)
        G-505700-001
    
 
    
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        Erfassungsdatum
        2015-04-01