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

被引：108
作者：
Howell, Gareth R.
Libby, Richard T.
Marchant, Jeffrey K.
Wilson, Lawriston A.
Cosma, Ioan M.
Smith, Richard S.
Anderson, Michael G.
John, Simon W. M.
机构：
[1] Jackson Lab, Bar Harbor, ME 04609 USA
[2] Tufts Univ, Dept Anat & Cell Biol, Boston, MA 02111 USA
[3] Howard Hughes Med Inst, Bar Harbor, ME USA
[4] Univ Iowa, Dept Physiol & Biophys, Iowa City, IA 52242 USA
[5] Tufts Univ, Dept Ophthalmol, Boston, MA 02111 USA
[6] Univ Rochester, Med Ctr, Inst Eye, Rochester, NY 14627 USA
来源：
BMC GENETICS | 2007年 / 8卷 / 1期
关键词：
D O I：
10.1186/1471-2156-8-45
中图分类号：
Q3 [遗传学];
学科分类号：
071007 ; 090102 ;
摘要：
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.
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页数：10
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