Nitric oxide is proangiogenic in the retina and choroid

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

Research output: Contribution to journalArticlepeer-review


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.

Original languageEnglish (US)
Pages (from-to)116-124
Number of pages9
JournalJournal of Cellular Physiology
Issue number1
StatePublished - 2002

ASJC Scopus subject areas

  • Physiology
  • Clinical Biochemistry
  • Cell Biology


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