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Abstract #6677 Published in IGR 4-1
Autoantibody against neuron-specific enolase found in glaucoma patients causes retinal dysfunction in vivo
Maruyama I; Maeda T; Okisaka S; Mizukawa A; Nakazawa M; Ohguro HJapanese Journal of Ophthalmology 2002; 46: 1-12
PURPOSE: In their recent paper, the authors reported the presence of serum autoantibody against neuron-specific enolase (NSE) in patients with glaucoma. The purpose of the present study was to investigate further the pathological effects of anti-NSE antibody on the retina by comparing them with the effects induced by N-methyl-D-aspartate (NMDA). METHODS: Either a glaucoma patient's serum, purified anti-NSE antibody, or 10-40 mM NMDA was intravitreously administered to Lewis rat eyes, and electrophysiological, histopathological, and biochemical evaluations were performed. In addition, the neuroprotective effects of anti-glaucoma drugs, such as timolol, betaxolol, nipradilol, and isopropyl unoprostone, and a calcium antagonist were also studied using these animal models. RESULTS: Electron microscopy revealed that intravitreal administration of a glaucoma patient's serum, which immunoreacted with retinal 50 kDa in Western blot analysis, and purified anti-NSE antibody induced retinal ganglion cell apoptosis in rat eyes. Functionally, these eyes showed a significant decrease of electroretinogram (ERG) responses and a remarkable decrease of rhodopsin phosphorylation reaction. These changes were comparable with the effects observed after the intravitreal administration of 20 mM NMDA. Co-administration of nipradilol, an α- and β-blocker, with anti-NSE antibody or 20 mM NMDA caused marked recovery of the affected ERG responses within two weeks. In contrast, administration of timolol or betaxolol showed no recovery effect on the ERG responses. Of these drugs, only betaxolol showed a recovery effect on NMDA-induced decrease of rhodopsin phosphorylation. Nilvadipine functioned beneficially on both impaired ERG and rhodopsin phosphorylation reactions observed in rat eyes injected intravitreously with anti-NSE antibody or NMDA. These effects of nilvadipine were not changed by the addition of endothelin-1. In contrast, isopropyl unoprostone had no effect on these functions. CONCLUSION: These observations suggest that serum autoantibody against NSE found in some patients with glaucoma induces retinal dysfunction in vivo, similarly to NMDA.
Dr. H. Ohguro, Department of Ophthalmology, Hirosaki University School of Medicine, 5 Zaifu-cho, Hirosaki, Aomori 036-8562, Japan
Classification:
5 Experimental glaucoma; animal models
9.2.2 Other risk factors for glaucoma (Part of: 9 Clinical forms of glaucomas > 9.2 Primary open angle glaucomas)
