Inducible nitric oxide synthase, Nos2, does not mediate optic neuropathy and retinopathy in the DBA/2J glaucoma model.

Inducible nitric oxide synthase, Nos2, does not mediate optic neuropathy and retinopathy in the DBA/2J glaucoma model. Research Abstract Details 

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Inducible nitric oxide synthase, Nos2, does not mediate optic neuropathy and retinopathy in the DBA/2J glaucoma model. Abstract Text:

Richard T Libby,Gareth R Howell,Iok-Hou Pang,Olga V Savinova,Adrienne K Mehalow,Joseph W Barter,Richard S Smith,Abbot F Clark,Simon W M John,Richard T Libby,Gareth R Howell,Iok-Hou Pang,Olga V Savinova,Adrienne K Mehalow,Joseph W Barter,Richard S Smith,Abbot F Clark,Simon W M John,

BACKGROUND: Nitric oxide synthase 2 (NOS2) contributes to neural death in some settings, but its role in glaucoma remains controversial. NOS2 is implicated in retinal ganglion cell degeneration in a rat glaucoma model in which intraocular pressure (IOP) is experimentally elevated by blood vessel cauterization, but not in a rat glaucoma model where IOP was elevated by injection of hypertonic saline. To test the importance of NOS2 for an inherited glaucoma, in this study we both genetically and pharmacologically decreased NOS2 activity in the DBA/2J mouse glaucoma model. METHODS: The expression of Nos2 in the optic nerve head was analyzed at both the RNA and protein levels at different stages of disease pathogenesis. To test the involvement of Nos2 in glaucomatous neurodegeneration, a null allele of Nos2 was backcrossed into DBA/2J mice and the incidence and severity of glaucoma was assessed in mice of each Nos2 genotype. Additionally, DBA/2J mice were treated with the NOS2 inhibitor aminoguanidine and the disease compared to untreated mice. RESULTS: Optic nerve head Nos2 RNA levels varied and increased during moderate but decreased at early and severe stages of disease. Despite the presence of a few NOS2 positive cells in the optic nerve head, NOS2 protein was not substantially increased during the glaucoma. Genetic deficiency of Nos2 or aminoguanidine treatment did not alter the IOP profile of DBA/2J mice. Additionally, neither Nos2 deficiency nor aminoguanidine had any detectable affect on the glaucomatous optic nerve damage. CONCLUSION: Glaucomatous neurodegeneration in DBA/2J mice does not require NOS2 activity. Further experiments involving various models are needed to assess the general importance of Nos2 in glaucoma.

Inducible nitric oxide synthase, Nos2, does not mediate optic neuropathy and retinopathy in the DBA/2J glaucoma model. Publishing Authors By Initials

RT Libby,GR Howell,IH Pang,OV Savinova,AK Mehalow,JW Barter,RS Smith,AF Clark,SW John,RT Libby,GR Howell,IH Pang,OV Savinova,AK Mehalow,JW Barter,RS Smith,AF Clark,SW John,

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Inducible nitric oxide synthase, Nos2, does not mediate optic neuropathy and retinopathy in the DBA/2J glaucoma model. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: BMC neuroscience

VOLUME: 8

Page Numbers: 108

Journal Abbreviation:

ISSN: 1471-2202

DAY: 19

MONTH: 12

YEAR: 2007

Inducible nitric oxide synthase, Nos2, does not mediate optic neuropathy and retinopathy in the DBA/2J glaucoma model. Information

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LANGUAGE: eng

NlmUniqueID: 100966986

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Grant and Affiliation Information for Inducible nitric oxide synthase, Nos2, does not mediate optic neuropathy and retinopathy in the DBA/2J glaucoma model.

AFFILIATION: The Jackson Laboratory, Bar Harbor, ME 04609, USA. Richard_Libby@URMC.rochester.edu

Country: England

AGENCY: United States NCI

GRANT: CA34196

ACRONYM: CA

MEDLINETA: BMC Neurosci

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