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
The Jackson Laboratory, Bar Harbor, Maine, USA.
BMC Genet. 2007 Jul 3;8:45. doi: 10.1186/1471-2156-8-45.
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.
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.
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.
青光眼是一组常见但尚未完全了解的疾病。DBA/2J小鼠会发生一种释放色素的虹膜疾病，最终导致眼压（IOP）升高和青光眼。我们之前已经表明，两个基因Gpnmb和Tyrp1中的突变引发了虹膜疾病。然而，随后眼压升高和视神经变性所涉及的机制仍不清楚。
在此，我们展示了具有正常功能的Gpnmb和/或Tyrp1基因且具有DBA/2J遗传背景的新小鼠品系。这些品系不会随着年龄增长而出现眼压升高或青光眼。
这些品系为使用DBA/2J小鼠研究青光眼的致病机制提供了急需的对照。鉴于Gpnmb和/或Tyrp1参与免疫、肿瘤发展和进展等领域，这些品系在其他研究领域也很重要。
