Expression of the inducible isoform of nitric oxide synthase in the retinas of human subjects with diabetes mellitus

Expression of the inducible isoform of nitric oxide synthase in the retinas of human subjects... PURPOSE: Inducible nitric oxide synthase has been implicated in the pathogenesis of cerebral ischemic damage, in the angiogenic process and in diabetic vascular damage. This study was undertaken to determine whether inducible nitric oxide synthase is present in the retinas from human subjects with diabetes mellitus. METHODS: This was an experimental immunohistochemical prospective study. Ten postmortem eyes from five subjects with diabetes mellitus, 10 eyes from five subjects without diabetes and without known ocular disease, and two eyes from one subject with unilateral ocular ischemic syndrome secondary to severe carotid artery obstruction were examined. We used immunohistochemical techniques and antibodies directed against inducible nitric oxide synthase, glial fibrillary acidic protein, and vimentin. The main outcome measure was immunoreactivity for these antibodies. RESULTS: Immunoreactivity for inducible nitric oxide synthase was not observed in retinas from all subjects without diabetes and without ocular disease. Six retinas from three subjects with diabetes and nonproliferative retinopathy, and the retina from the eye with ocular ischemic syndrome showed immunoreactivity for inducible nitric oxide synthase in cells with elongated processes. Based on morphology and on glial fibrillary acidic protein and vimentin immunoreactivity, this inducible nitric oxide synthase immunoreactivity appeared to localize to retinal Müller glial cells. CONCLUSIONS: These observations suggest that Müller cells may be involved in the microvascular remodeling of the diseased retina and that high concentrations of nitric oxide produced by inducible nitric oxide synthase could contribute to neurotoxicity and angiogenesis that occur in diabetic retinopathy. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png American Journal of Ophthalmology Elsevier

Expression of the inducible isoform of nitric oxide synthase in the retinas of human subjects with diabetes mellitus

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Publisher
Elsevier
Copyright
Copyright © 2001 Elsevier Science Inc.
ISSN
0002-9394
D.O.I.
10.1016/S0002-9394(01)01127-8
Publisher site
See Article on Publisher Site

Abstract

PURPOSE: Inducible nitric oxide synthase has been implicated in the pathogenesis of cerebral ischemic damage, in the angiogenic process and in diabetic vascular damage. This study was undertaken to determine whether inducible nitric oxide synthase is present in the retinas from human subjects with diabetes mellitus. METHODS: This was an experimental immunohistochemical prospective study. Ten postmortem eyes from five subjects with diabetes mellitus, 10 eyes from five subjects without diabetes and without known ocular disease, and two eyes from one subject with unilateral ocular ischemic syndrome secondary to severe carotid artery obstruction were examined. We used immunohistochemical techniques and antibodies directed against inducible nitric oxide synthase, glial fibrillary acidic protein, and vimentin. The main outcome measure was immunoreactivity for these antibodies. RESULTS: Immunoreactivity for inducible nitric oxide synthase was not observed in retinas from all subjects without diabetes and without ocular disease. Six retinas from three subjects with diabetes and nonproliferative retinopathy, and the retina from the eye with ocular ischemic syndrome showed immunoreactivity for inducible nitric oxide synthase in cells with elongated processes. Based on morphology and on glial fibrillary acidic protein and vimentin immunoreactivity, this inducible nitric oxide synthase immunoreactivity appeared to localize to retinal Müller glial cells. CONCLUSIONS: These observations suggest that Müller cells may be involved in the microvascular remodeling of the diseased retina and that high concentrations of nitric oxide produced by inducible nitric oxide synthase could contribute to neurotoxicity and angiogenesis that occur in diabetic retinopathy.

Journal

American Journal of OphthalmologyElsevier

Published: Oct 1, 2001

References

  • Temporal characteristics of the protective effect of aminoguanidine on cerebral ischemic damage
    Zhang, F; Iadecola, C
  • Cerebellar stimulation reduces inducible nitric oxide synthase expression and protects brain from ischemia
    Gales, E; Golanov, E.V; Feinstein, D.L; Kobylarz, K.A; Glickstein, S.B; Reis, D.J
  • Expression of inducible nitric oxide synthase immunoreactivity in rat brain following chronic hypoxia
    Niwa, K; Takizawa, S; Kawaguchi, C; Kamiya, U; Kuwahira, I; Shinohara, Y
  • Nitric oxide mediates mitogenic effect of VEGF on coronary venular endothelium
    Morbidelli, L; Chang, C.H; Douglas, J.G; Granger, H.J; Ledda, F; Ziche, M
  • The role of nitric oxide synthase isoforms and arginase in the pathogenesis of diabetic foot ulcers
    Jude, E.B; Boulton, A.J; Ferguson, M.W; Appleton, I
  • Elevated vitreous nitric oxide levels in patients with proliferative diabetic retinopathy
    Yilmaz, G; Esser, P; Kociek, N; Aydin, P; Heimann, K
  • Nitric oxide neurotoxicity
    Dawson, V.L; Dawson, T.M
  • Secondary intervention with aminoguanidine retards the progression of diabetic retinopathy in the rat model
    Hames, H.P; Strodter, D; Weiss, A; Bretzel, R.G; Federlin, K; Brownlee, M

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