| First Author | Ding K | Year | 2005 |
| Journal | Invest Ophthalmol Vis Sci | Volume | 46 |
| Issue | 3 | Pages | 1010-6 |
| PubMed ID | 15728559 | Mgi Jnum | J:96396 |
| Mgi Id | MGI:3530393 | Doi | 10.1167/iovs.04-0788 |
| Citation | Ding K, et al. (2005) Retinal Disease in Mice Lacking Hypoxia-Inducible Transcription Factor-2{alpha}. Invest Ophthalmol Vis Sci 46(3):1010-6 |
| abstractText | PURPOSE: To characterize ocular disease in HIF-2alpha-null mice. METHODS: Histologic, electroretinographic (ERG), and molecular studies were performed on samples obtained from age- and gender-matched HIF-2alpha-null (HIF-2alpha-KO), HIF-2alpha-heterozygous (HIF-2alpha-HET), and wild-type (WT) littermate mice. RESULTS: HIF-2alpha-KO mice exhibited marked thinning of the retina and abnormal retinal vasculature. The pathologic changes in HIF-2alpha-KO mice were associated with a virtual absence of postreceptor function. The expression of a surrogate marker for HIF-2alpha mRNA localized to vascular endothelial, amacrine, and retinal pigment epithelial (RPE) cells. Several HIF-2alpha target genes involved in angiogenesis, retinal protection, and stress responses have altered expression patterns in HIF-2alpha-KO retinas. CONCLUSIONS: HIF-2alpha-KO mice exhibit marked retinopathy consistent with complete loss of vision by 1 month of age. Impaired HIF-2alpha signaling in HIF-2alpha-KO mice likely produces functional deficits in cell types in which HIF-2alpha 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-2alpha-KO mice. |
