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Editors Selection IGR 18-1
Basic research: Eyes of DBA/2J mice
Comment by Art Neufeld on:
20684 Inducible nitric oxide synthase, Nos2, does not mediate optic neuropathy and retinopathy in the DBA/2J glaucoma model., Libby RT; Howell GR; Pang IH et al., BMC Neuroscience, 2007; 8: 108
The eyes of DBA/2J mice have a lot of problems. From reviewing a large body of publications, these eyes, with age, develop iris atrophy, iris pigment dispersion, cataract, anterior synechia, release of toxic intermediates from the melanin synthesis pathway, corneal haziness and calcification, loss of immune privilege, inflammation, an inability to inhibit T cell activation, immunological changes, increased synthesis of IL-18 and MMP-2, deposits of amyloid-β, breech of the blood-ocular barriers, unregulated microglia, Muller-cell activation, signs of neovascularization, decreased synthesis of kynurenuc acid, elevated retinal concentrations of glutamate, glutamine, glycine, alanine, lysine and arginine, modest elevation of IOP, an unpredictable loss of retinal ganglion cells (RGCs) and, perhaps, a secondary glaucoma. By linking elevated IOP + loss of RGCs in the literature, the use of these mice as a model of glaucoma has been touted by the originators of the link while ignoring any of the myriad of other changes in the eye that could be responsible for, or contribute to, loss of RGCs. Certainly, the ability to prevent loss of RGCs with high-dose γ-irradiation and bone marrow transplant strongly indicates immunological responses in the death of RGCs.
Recently published data on the DBA/2J mice show that elevated IOP and loss of RGCs do not always occur in the same animal, that elevated IOP and loss of RGCs can be uncoupled and that loss of the RGC cell body precedes loss of axons of the optic nerve.
The eyes of DBA/2J mice have a lot of problemsConsidering the extent of pathological changes occurring in the eyes of DBA/2J mice, why selectively hypothesize an involvement of NOS-2 in the loss of RGCs in these mice? I could have performed these experiments in my laboratory, but the DBA/2J mouse is not 'clean' as a glaucoma model and the experiments reported in this paper are not worth the time and effort. I agree with Libby et al. (127) that 'further experiments involving various models are needed to assess the general importance of NOS-2 in glaucoma'. However, sufficient research has been done on the DBA/2J mice to stop referring to these mice as a model of glaucoma.
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