Absence of glaucoma in DBA/2J mice homozygous for wild-type versions of Gpnmb and Tyrp1.
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.


CONCLUSIONS
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.
Howell
Gareth R
GR
The Jackson Laboratory, Bar Harbor, Maine, USA. gareth.howell@jax.org <gareth.howell@jax.org>
Libby
Richard T
RT
Marchant
Jeffrey K
JK
Wilson
Lawriston A
LA
Cosma
Ioan M
IM
Smith
Richard S
RS
Anderson
Michael G
MG
John
Simon W M
SW
D000818:Animals; D005136:Eye Proteins / Q000235:genetics*; D005838:Genotype; D005901:Glaucoma / Q000209:etiology / Q000235:genetics* / Q000473:pathology; D006720:Homozygote; D007429:Intraocular Pressure / Q000235:genetics*; D007499:Iris Diseases / Q000150:complications / Q000235:genetics / Q000473:pathology; D008562:Membrane Glycoproteins / Q000235:genetics*; D051379:Mice; D008811:Mice, Inbred DBA; D008817:Mice, Mutant Strains; D009900:Optic Nerve / Q000473:pathology; D010088:Oxidoreductases / Q000235:genetics*
D005136:Eye Proteins; C445671:Gpnmb protein, mouse; D008562:Membrane Glycoproteins; D010088:Oxidoreductases; C079621:Tyrp1 protein, mouse