April 2011
Volume 52, Issue 14
ARVO Annual Meeting Abstract  |   April 2011
Genetic Control Of Avascular Area In Mouse Oxygen-induced Retinopathy
Author Affiliations & Notes
  • Bliss E. O'Bryhim
    Molecular & Integrative Physiology,
    Univ of Kansas Medical Center, Kansas City, Kansas
  • Jeff Radel
    Occupational Therapy Education,
    Univ of Kansas Medical Center, Kansas City, Kansas
  • R. C. Andrew Symons
    Univ of Kansas Medical Center, Kansas City, Kansas
  • Footnotes
    Commercial Relationships  Bliss E. O'Bryhim, None; Jeff Radel, None; R. C. Andrew Symons, None
  • Footnotes
    Support  Kansas Lions Sight Foundation, Knights Templar Eye Foundation
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 3988. doi:
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      Bliss E. O'Bryhim, Jeff Radel, R. C. Andrew Symons; Genetic Control Of Avascular Area In Mouse Oxygen-induced Retinopathy. Invest. Ophthalmol. Vis. Sci. 2011;52(14):3988.

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      © ARVO (1962-2015); The Authors (2016-present)

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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 

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