Abstract
Purpose: :
To investigate the genetic control of retinal avascular area in mouse oxygen induced retinopathy.
Methods: :
We determined the retinal avascular area at post-natal day 16 in C57BL/6ByJ, BALB/cByJ, offspring of reciprocal F1 crosses, and 220 F2 mice that were subjected to the oxygen induced retinopathy (OIR) protocol. A genome-wide scan was performed of selected albino and non-albino mice to determine quantitative trait loci associated with weight and avascular area.
Results: :
C57BL/6ByJ mice had significantly larger avascular areas than BALB/cByJ (p < 0.005). The phenotype of the F1 mice was intermediate between that of the parental strains. Albino mice of the F2 generation had smaller avascular areas than the non-albino mice (p < 5 x 10-12). A quantitative trait locus for weight was mapped to chromosome 5 (LOD = 4.51, p = 0.02 (empirical genome-wide threshold)). A quantitative trait locus for retinal avascular area was found on chromosome 9 (LOD = 3.86, p = 0.07).
Conclusions: :
Retinal avascular area in the mouse oxygen-induced retinopathy model is under genetic control. Further experiments will reveal whether the quantitative trait loci described here control vaso-obliteration or vascular regeneration, and will seek to identify the quantitative trait genes that modify these phenotypes.
Keywords: retinopathy of prematurity • gene modifiers • retinal neovascularization