Involvement of CD24 in angiogenesis in a mouse model of oxygen-induced retinopathy

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.

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.

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.

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.