February 1996
Volume 37, Issue 2
Free
Articles  |   February 1996
Corn1: a mouse model for corneal surface disease and neovascularization.
Author Affiliations
  • R S Smith
    Jackson Laboratory, Bar Harbor, Maine 04609-1500, USA.
  • N L Hawes
    Jackson Laboratory, Bar Harbor, Maine 04609-1500, USA.
  • S D Kuhlmann
    Jackson Laboratory, Bar Harbor, Maine 04609-1500, USA.
  • J R Heckenlively
    Jackson Laboratory, Bar Harbor, Maine 04609-1500, USA.
  • B Chang
    Jackson Laboratory, Bar Harbor, Maine 04609-1500, USA.
  • T H Roderick
    Jackson Laboratory, Bar Harbor, Maine 04609-1500, USA.
  • J P Sundberg
    Jackson Laboratory, Bar Harbor, Maine 04609-1500, USA.
Investigative Ophthalmology & Visual Science February 1996, Vol.37, 397-404. doi:
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      R S Smith, N L Hawes, S D Kuhlmann, J R Heckenlively, B Chang, T H Roderick, J P Sundberg; Corn1: a mouse model for corneal surface disease and neovascularization.. Invest. Ophthalmol. Vis. Sci. 1996;37(2):397-404.

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

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Abstract

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 of 8 months of age by routine techniques of light microscopic 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, development of stromal neovascularization by 20 days of age, and cataract by 48 days of age. Corneal epithelial cell kinetics demonstrated prominent labelling 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.

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