| First Author | Smith RS | Year | 1996 |
| Journal | Invest Ophthalmol Vis Sci | Volume | 37 |
| Issue | 2 | Pages | 397-404 |
| PubMed ID | 8603845 | Mgi Jnum | J:31798 |
| Mgi Id | MGI:79292 | Citation | Smith RS, et al. (1996) Corn1: a mouse model for corneal surface disease and neovascularization. Invest Ophthalmol Vis Sci 37(2):397-404 |
| abstractText | Purpose. To describe a new mouse model of corneal surface disease and neovascularization. Methods. Anatomic changes were demonstrated in corn1 and control A.By/SnJ mice from day 10 of gestation to 8 months of age by routine techniques of light microscopy and scanning electron microscopy. Corneal epithelial cell kinetics were evaluated by labeling cells in the ''S'' phase of the cell cycle by intraperitoneal injection of tritiated thymidine. Labeled cells were counted under 250X magnification, and the length of the corneal epithelial chord was measured by morphometric techniques. Results were expressed as labeled cells per linear millimeter of corneal epithelium. The corn1 locus was mapped using selected back-crosses. Results. Corn1 is characterized by early, irregular thickening of the corneal epithelium, develop ment of stromal neovascularization by 20 days of age, and cataract by 48 days of age. Corneal epithelial cell kinetics demonstrated prominent labeling of corn1 mice at 30 days of age compared to the control mice. Corn1 behaves as an autosomal recessive gene and is located on mouse chromosome 2, approximately 5.2 cM from the agouti locus. Heterozygotes have no corneal disease. Conclusions, Corn1 mice, with genetically determined corneal epithelial hyperplasia and stromal neovascularization, may be particularly useful in studies of neovascularization and corneal surface proliferative disease. |
