May 2003
Volume 44, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2003
Inducible Nitric Oxide Synthase (Nos2) is Not Required for Glacuomatous Optic Nerve Damage in DBA/2J Mice
Author Affiliations & Notes
  • R.T. Libby
    The Jackson Laboratory, Bar Harbor, ME, United States
  • R.S. Smith
    The Howard Hughes Medical Institute and The Jackson Laboratory, Bar Harbor, ME, United States
  • O.V. Savinova
    The Howard Hughes Medical Institute and The Jackson Laboratory, Bar Harbor, ME, United States
  • A.F. Clark
    Glaucoma Research, Alcon Research, Ltd., Fort Worth, TX, United States
  • S.W. John
    Glaucoma Research, Alcon Research, Ltd., Fort Worth, TX, United States
  • Footnotes
    Commercial Relationships  R.T. Libby, None; R.S. Smith, None; O.V. Savinova, None; A.F. Clark, Alcon Research, Ltd E; S.W.M. John, None.
  • Footnotes
    Support  Howard Hughs Medical Institute (SWJ) Alcon Research, Ltd (AFC)
Investigative Ophthalmology & Visual Science May 2003, Vol.44, 145. doi:
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      R.T. Libby, R.S. Smith, O.V. Savinova, A.F. Clark, S.W. John; Inducible Nitric Oxide Synthase (Nos2) is Not Required for Glacuomatous Optic Nerve Damage in DBA/2J Mice . Invest. Ophthalmol. Vis. Sci. 2003;44(13):145.

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

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Abstract

Abstract: : Purpose: Inducible nitric oxide synthase (Nos2 (formerly iNos)) was previously implicated in retinal ganglion cell degeneration induced by elevated intraocular pressure (IOP) in a rat model where IOP is artificially raised. DBA/2J mice develop spontaneous, chronic, and pathologically elevated IOP as a consequence of an iris disease involving pigment dispersion and stromal atrophy. Using the DBA/2J mouse glaucoma model, we test the hypothesis that Nos2 is necessary for glaucomatous retinal ganglion cell death. Methods: A null allele of Nos2 was backcrossed into DBA/2J mice for 13 generations. All experimental mice were clinically assessed at multiple ages and IOPs were measured at several ages. Optic nerves were harvested from Nos2 wild type, heterozygous and homozygous mutant mice at two times points subsequent to intraocular pressure elevation, 10 and 11 months. Optic nerves were sectioned and stained with paraphenylenediamine, which darkly stains the axoplasm of sick or dying axons. Optic nerve damage was determined using a 5 point grading scheme (1 = no damage, 5 = destroyed optic nerve). Results: Nos2 deficiency did not alter the progression of the iris disease or pressure elevation. Similarly, Nos2 deficiency did not alter optic nerve damage in homozygous mutant and heterozygous mice. Optic nerve damage scores for Nos2 wild type and homozygous mutant mice were: 10 months, wild type 3.0 ± 0.39 (mean ± SEM; n = 16), homozygous mutant 3.4 ± 0.47 (n = 15), P = 0.5; 11 months, wild type 4.18 ± 0.38 (n = 11), homozygous mutant 3.92 ± 0.29 (n = 13), P = 0.6. Conclusion: These data clearly show that Nos2 is not required for glaucomatous optic nerve damage in DBA/2J mice. Further experiments involving various models are needed to assess the general importance of Nos2 in glaucomatous nerve damage.

Keywords: animal model • nitric oxide • genetics 
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