Abstract |
Nitric oxide (NO) has been shown to have proangiogenic or antiangiogenic effects depending upon the setting. In this study, we used mice with targeted deletion of one of the three isoforms of nitric oxide synthase (NOS) to investigate the effects of NO in ocular neovascularization. In transgenic mice with increased expression of vascular endothelial growth factor ( VEGF) in photoreceptors, deficiency of any of the three isoforms caused a significant decrease in subretinal neovascularization, but no alteration of VEGF expression. In mice with laser-induced rupture of Bruch's membrane, deficiency of inducible NOS (iNOS) or neuronal NOS (nNOS), but not endothelial NOS (eNOS), caused a significant decrease in choroidal neovascularization. In mice with oxygen-induced ischemic retinopathy, deficiency of eNOS, but not iNOS or nNOS caused a significant decrease in retinal neovascularization and decreased expression of VEGF. These data suggest that NO contributes to both retinal and choroidal neovascularization and that different isoforms of NOS are involved in different settings and different disease processes. A broad spectrum NOS inhibitor may have therapeutic potential for treatment of both retinal and choroidal neovascularization.
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Authors | Akira Ando, Amy Yang, Keisuke Mori, Haruhiko Yamada, Eri Yamada, Kyoichi Takahashi, Jina Saikia, Min Kim, Michele Melia, Mark Fishman, Paul Huang, Peter A Campochiaro |
Journal | Journal of cellular physiology
(J Cell Physiol)
Vol. 191
Issue 1
Pg. 116-24
(Apr 2002)
ISSN: 0021-9541 [Print] United States |
PMID | 11920687
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)
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Copyright | Copyright 2002 Wiley-Liss, Inc. |
Chemical References |
- Nitric Oxide
- Nitric Oxide Synthase
- Nitric Oxide Synthase Type I
- Nitric Oxide Synthase Type II
- Nitric Oxide Synthase Type III
- Nos1 protein, mouse
- Nos2 protein, mouse
- Nos3 protein, mouse
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Topics |
- Animals
- Bruch Membrane
(radiation effects)
- Choroid
(blood supply)
- Ischemia
(physiopathology)
- Lasers
- Mice
- Mice, Knockout
(genetics)
- Neovascularization, Pathologic
(etiology)
- Nitric Oxide
(physiology)
- Nitric Oxide Synthase
(deficiency, genetics)
- Nitric Oxide Synthase Type I
- Nitric Oxide Synthase Type II
- Nitric Oxide Synthase Type III
- Retinal Vessels
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