title: Vascular endothelial growth factor-B and retinal vascular development in the mouse.
abstract: OBJECTIVE
  Vascular endothelial growth factor-A (VEGF-A) is crucial to retinal vascular growth, both normal and pathological. VEGF-B, recently characterized, is reported to be expressed in retinal tissues, but the importance of VEGF-B to retinal vascular development remained unknown. The aim of this study was to analyse retinal vascular growth in the Vegfb-/- knockout mouse.
  
  
  METHODS
  Retinal vascular growth was measured in Vegfb-/- knockout mice raised under normal conditions, and Vegfb-/- knockout mice with an oxygen-induced proliferative retinopathy. Wild type Vegfb+/+ mice served as controls. Vessels were perfused with ink and retinal flatmounts secondarily labelled with FITC-lectin (BS-1, Griffonia simplicifolia). Area and diameter of retinal growth and retinal vascular growth were recorded over days 0-20, and capillary density and mean diameter recorded from day 17 pups.
  
  
  RESULTS
  A variety of techniques confirmed that Vegfb+/+ mice expressed VEGF-B and that VEGF-B expression was absent in Vegfb-/- mice. Vegfb-/- mice raised in room air showed no significant differences from Vegfb+/+ controls. No differences were found in oxygen-induced retinopathy between Vegfb-/- and Vegfb+/+ pups in either the extent of the initial oxygen-induced ablation, or in the regrowth of retinal vessels or vitreal (neovascular) sprouts; vitreal sprouts are important markers of the abnormal proliferative response, and are maximally expressed on day 17 in this model of oxygen-induced retinopathy.
  
  
  CONCLUSIONS
  These results indicate that a lack of VEGF-B does not significantly affect development of the retinal vasculature under normal conditions, nor does it appear to affect the proliferative retinal responses seen in oxygen-induced retinopathy.
authors.affiliation: School of Health Science, Griffith University Gold Coast, Southport, Australia.
authors.forename: Melissa
authors.initials: M
authors.lastname: Reichelt
authors.forename: Shunning
authors.initials: S
authors.lastname: Shi
authors.forename: Mark
authors.initials: M
authors.lastname: Hayes
authors.forename: Graham
authors.initials: G
authors.lastname: Kay
authors.forename: Jennifer
authors.initials: J
authors.lastname: Batch
authors.forename: Glen A
authors.initials: GA
authors.lastname: Gole
authors.forename: Jay
authors.initials: J
authors.lastname: Browning
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D004195:Disease Models, Animal; D016228:Endothelial Growth Factors / Q000235:genetics / Q000502:physiology*; D006801:Humans; D018496:Hyperoxia / Q000150:complications; D007231:Infant, Newborn; D051379:Mice; D018345:Mice, Knockout; D010100:Oxygen / Q000633:toxicity; D012333:RNA, Messenger / Q000378:metabolism; D015861:Retinal Neovascularization / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology*; D012171:Retinal Vessels / Q000254:growth & development* / Q000378:metabolism; D012178:Retinopathy of Prematurity / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D042561:Vascular Endothelial Growth Factor B
chemical_list: D016228:Endothelial Growth Factors; D012333:RNA, Messenger; D042561:Vascular Endothelial Growth Factor B; D010100:Oxygen