Purpose:
Retinopathy of prematurity (ROP) is a common cause of blindnessin children. The development and severity of ROP is known tobe influenced by gestational age at delivery, birth weight,and over-use of oxygen in the nursery. It is unknown whethergenetic factors influence ROP severity. This study aims to usethe mouse genetics to identify genes which play a role in thedevelopment of oxygen induced retinopathy (OIR), a model ofROP.
Methods:
A mapping cross was established between BALB/cByJ and C57BL/6ByJ,which are, respectively, relatively resistant and susceptibleto central retinal vaso-obliteration in the OIR model. So far,111 neonatal F2 mice, out of a planned 200, have been subjectedto 120 hours of 75% inspired O2, beginning on day 7 of neonatallife. 96 hours after the return to room air, mice were anesthetized,perfused with fluorescein-isothiocyanate (FITC)-labeled dextranand enucleated. Retinas were excised and flat-mounted, and theavascular area was measured using ImageJ software.
Results:
Susceptibility to the development of ROP was not shown to beassociated with sex(p > 0.05), but was shown to correlatewith weight at P16 (p < 10-15) and with albino versus non-albinocoat color (p <10-5).
Conclusions:
In this cross, mouse weight and allelotype at the tyrosinaselocus were associated with susceptibility to vaso-obliteration.However, these factors explain only a small proportion of thetotal variation, and it is expected that whole genome analysiswill lead to the discovery of further loci.
Keywords: retinopathy of prematurity • gene mapping • neovascularization