April 1999
Volume 40, Issue 5
Free
Articles  |   April 1999
The contribution of various NOS gene products to HIV-1 coat protein (gp120)-mediated retinal ganglion cell injury.
Author Affiliations
  • E B Dreyer
    Department of Ophthalmology, Scheie Eye Institute, Philadelphia Veterans Administration, University of Pennsylvania, USA.
  • D Zurakowski
    Department of Ophthalmology, Scheie Eye Institute, Philadelphia Veterans Administration, University of Pennsylvania, USA.
  • M Gorla
    Department of Ophthalmology, Scheie Eye Institute, Philadelphia Veterans Administration, University of Pennsylvania, USA.
  • C K Vorwerk
    Department of Ophthalmology, Scheie Eye Institute, Philadelphia Veterans Administration, University of Pennsylvania, USA.
  • S A Lipton
    Department of Ophthalmology, Scheie Eye Institute, Philadelphia Veterans Administration, University of Pennsylvania, USA.
Investigative Ophthalmology & Visual Science April 1999, Vol.40, 983-989. doi:
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      E B Dreyer, D Zurakowski, M Gorla, C K Vorwerk, S A Lipton; The contribution of various NOS gene products to HIV-1 coat protein (gp120)-mediated retinal ganglion cell injury.. Invest. Ophthalmol. Vis. Sci. 1999;40(5):983-989.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

PURPOSE: There is growing evidence that the neuronal pathology seen with HIV-1 is mediated, at least in part, through an excitotoxic/free radical pathway. Nitric oxide (NO) plays a critical role in the nervous system, in both normal and pathologic states, and appears to be involved in a variety of excitotoxic pathways. Whether isoforms of nitric oxide synthase (NOS) are involved in gp120-mediated neuronal loss in the retina was therefore explored. METHODS: To determine which (if any) of the various isoforms of NOS are critical in gp120-mediated damage in the retina, neuronal NOS-deficient [nNOS(-/-)], endothelial NOS-deficient [eNOS(-/ -)], and immunologic NOS-deficient [iNOS(-/-)] mice were subjected to intravitreal injections of gp120. RESULTS: Retinal ganglion cells in the nNOS(-/-) mouse were relatively resistant to gp120, manifesting attenuation of gp120-induced injury compared with wild-type mice. The iNOS(-/-) and eNOS(-/-) mice were as susceptible to gp120 toxicity as control animals. NOS inhibitors were protective against this toxicity. CONCLUSIONS: The presence of nNOS is a prerequisite for the full expression of gp120-mediated loss in the retina; eNOS and iNOS do not appear to play a significant role.

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