Title

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

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.