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(Investigative Ophthalmology and Visual Science. 2005;46:1010-1016.)
© 2005 by The Association for Research in Vision and Ophthalmology, Inc.
DOI:  10.1167/iovs.04-0788
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Retinal Disease in Mice Lacking Hypoxia-Inducible Transcription Factor-2{alpha}

Kan Ding,1 Marzia Scortegagna,1 Robyn Seaman,2 David G. Birch,2,3 and Joseph A. Garcia1

1From the Departments of Internal Medicine and 3Ophthalmology, University of Texas Southwestern Medical Center, Dallas, Texas; and the 2Retina Foundation of the Southwest, Dallas, Texas.

PURPOSE. To characterize ocular disease in HIF-2{alpha}-null mice.

METHODS. Histologic, electroretinographic (ERG), and molecular studies were performed on samples obtained from age- and gender-matched HIF-2{alpha}-null (HIF-2{alpha}-KO), HIF-2{alpha}-heterozygous (HIF-2{alpha}-HET), and wild-type (WT) littermate mice.

RESULTS. HIF-2{alpha}-KO mice exhibited marked thinning of the retina and abnormal retinal vasculature. The pathologic changes in HIF-2{alpha}-KO mice were associated with a virtual absence of postreceptor function. The expression of a surrogate marker for HIF-2{alpha} mRNA localized to vascular endothelial, amacrine, and retinal pigment epithelial (RPE) cells. Several HIF-2{alpha} target genes involved in angiogenesis, retinal protection, and stress responses have altered expression patterns in HIF-2{alpha}-KO retinas.

CONCLUSIONS. HIF-2{alpha}-KO mice exhibit marked retinopathy consistent with complete loss of vision by 1 month of age. Impaired HIF-2{alpha} signaling in HIF-2{alpha}-KO mice likely produces functional deficits in cell types in which HIF-2{alpha} normally is expressed, ultimately resulting in retinopathy. Future studies will address whether the molecular abnormalities described in this study are directly responsible for the retinal disease in HIF-2{alpha}-KO mice.




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