Absence of glaucoma in DBA/2J mice homozygous for wild-type versions of Gpnmb and Tyrp1.
Document Type
Article
Publication Date
2007
Keywords
Eye-Proteins, Genotype, Glaucoma, Homozygote, Intraocular-Pressure, Iris-Diseases, Membrane-Glycoproteins, Mice-Inbred-DBA, Mice-Mutant-Strains, Optic-Nerve, Oxidoreductases
First Page
45
Last Page
45
JAX Source
BMC Genet 2007; 8:45.
Abstract
BACKGROUND: The glaucomas are a common but incompletely understood group of diseases. DBA/2J mice develop a pigment liberating iris disease that ultimately causes elevated intraocular pressure (IOP) and glaucoma. We have shown previously that mutations in two genes, Gpnmb and Tyrp1, initiate the iris disease. However, mechanisms involved in the subsequent IOP elevation and optic nerve degeneration remain unclear. RESULTS: Here we present new mouse strains with Gpnmb and/or Tyrp1 genes of normal function and with a DBA/2J genetic background. These strains do not develop elevated IOP or glaucoma with age. CONCLUSION: These strains provide much needed controls for studying pathogenic mechanisms of glaucoma using DBA/2J mice. Given the involvement of Gpnmb and/or Tyrp1 in areas such as immunology and tumor development and progression, these strains are also important in other research fields.
Recommended Citation
Howell GR,
Libby RT,
Marchant JK,
Wilson LA,
Cosma IM,
Smith RS,
Anderson MG,
John SW.
Absence of glaucoma in DBA/2J mice homozygous for wild-type versions of Gpnmb and Tyrp1. BMC Genet 2007; 8:45.