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Editors Selection IGR 18-1

Basic research: Nitric oxide synthase

Comment by Art Neufeld on:

11926 Evaluation of inducible nitric oxide synthase in glaucomatous optic neuropathy and pressure-induced optic nerve damage, Pang IH; Johnson EC; Jia L et al., Investigative Ophthalmology and Visual Science, 2005; 46: 1313-1321

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The publication of Pang et al. (88) presents laboratory data and comes to the conclusion that inducible nitric oxide synthase (NOS-2, iNOS) is not responsible for the optic neuropathy in glaucoma. Nevertheless, there is a significant literature using a variety of techniques that supports the hypothesis that excessive NO, made by NOS-2 in astrocytes of the optic nerve head, is damaging to the axons of the retinal ganglion cells in glaucoma.2 Compared to previous reports that studied NOS-2 in glaucoma, Pang et al. used a different rat model, an ambiguous method to measure exposure to elevated IOP, a semi-quantitative method to assess retinal ganglion cell loss and other differences from reported methods. Whereas the authors' conclusion may be correct for the experiments that they performed, the authors have made a generalized, overstated, conclusion based on their assumptions that all animal models and all methods must give the same answer. In fact, the underlying mechanisms in different models need not be similar and all methods are not equivalent. Indeed, not all glaucoma patients are the same:

• Certainly, there are several cellular mechanisms that can cause the decrease in aqueous humor outflow facility that increases intraocular pressure in glaucoma patients.
• Undoubtedly, there is not one cellular mechanism, and only one mechanism, that accounts for the degeneration of the axons of the optic nerve in glaucoma patients.
• Clearly, all glaucoma patients do not respond in an identical manner to a given glaucoma medication.

The investigators collaborating in Pang et al. have published numerous papers, but have not put forth a mechanism for glaucomatous optic neuropathy and retinal ganglion cell death. Workers in the field look forward to seeing these investigators use their considerable technical resources to discover a viable mechanism that may be of use for treating glaucoma patients. After all, why else are we doing research?

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