title: Involvement of CD24 in angiogenesis in a mouse model of oxygen-induced retinopathy.
abstract: OBJECTIVE
  To investigate a possible involvement of CD24 in vascular remodeling and angiogenesis in retinopathy of prematurity (ROP) in a mouse model of oxygen-induced retinopathy.
  
  
  METHODS
  17 CD24 knockout (KO) and 12 wild-type (WT) C57BL/6 mice were used. Group 1 mice were exposed to oxygen concentrations of 75 ± 2% from postnatal day (P) 7 to P12. Group 2 mice were raised in room air. At P17, all mice underwent fluorescein-conjugated-dextran perfusion and were sacrificed. The flat-mounted retinas were scored manually and digitally by a new computerized algorithm, according to blood vessel obliteration, tortuosity, vascular tufts and neovascularization formation.
  
  
  RESULTS
  Fifty four retinal whole mounts were available for analysis and scoring. Group 1 retinas had significantly higher values of vaso-obliteration, tufts, neovascularization, vessel tortuosity and higher mean retinopathy scores than Group 2 retinas (KO mice: 9.0 ± 0.27 vs. 0.74 ± 0.2, respectively, P < 0.0001; WT mice: 7.58 ± 0.40 vs. 1.17 ± 0.27, respectively, P < 0.0001). Manual scoring in Group 1 revealed higher values of neovascularization, tortuosity and mean retinopathy scores in KO mice vs. WT mice (9.0 ± 0.27 vs. 7.58 ± 0.40, respectively, P = 0.009). Digital scoring revealed a higher neovascularization score in KO mice as well (13.72 ± 0.82% vs. 8.06 ± 0.27%, P < 0.0001). All mice had similar vaso-obliteration areas. There were no significant differences between KO and WT mice in Group 2.
  
  
  CONCLUSIONS
  Absence of CD24 may have a deleterious effect on angiogenesis occurring in the second stage of ROP development, though its role in vessel obliteration during the first stage of ROP is probably limited.
authors.affiliation: Department of Ophthalmology,Tel-Aviv Medical Center, Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel.
authors.forename: Hadas
authors.initials: H
authors.lastname: Newman
authors.forename: Shiran
authors.initials: S
authors.lastname: Shapira
authors.forename: Oriel
authors.initials: O
authors.lastname: Spierer
authors.forename: Sarah
authors.initials: S
authors.lastname: Kraus
authors.forename: Mordechai
authors.initials: M
authors.lastname: Rosner
authors.forename: Sarah
authors.initials: S
authors.lastname: Pri-Chen
authors.forename: Anat
authors.initials: A
authors.lastname: Loewenstein
authors.forename: Nadir
authors.initials: N
authors.lastname: Arber
authors.forename: Adiel
authors.initials: A
authors.lastname: Barak
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D051927:CD24 Antigen / Q000502:physiology*; D003911:Dextrans / Q000378:metabolism; D004195:Disease Models, Animal; D005452:Fluoresceins / Q000378:metabolism; D006801:Humans; D018496:Hyperoxia / Q000378:metabolism / Q000503:physiopathology; D007231:Infant, Newborn; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D010100:Oxygen / Q000633:toxicity; D015861:Retinal Neovascularization / Q000378:metabolism* / Q000503:physiopathology; D012171:Retinal Vessels / Q000473:pathology*; D012178:Retinopathy of Prematurity / Q000378:metabolism* / Q000503:physiopathology
chemical_list: D051927:CD24 Antigen; C497890:Cd24a protein, mouse; D003911:Dextrans; D005452:Fluoresceins; C052526:fluorescein-dextran; D010100:Oxygen