Inducible nitric oxide synthase, , does not mediate optic neuropathy and retinopathy in the DBA/2J glaucoma model-3

<p><b>Copyright information:</b></p><p>Taken from "Inducible nitric oxide synthase, , does not mediate optic neuropathy and retinopathy in the DBA/2J glaucoma model"</p><p>http://www.biomedcentral.com/1471-2202/8/108</p><p>BMC Neuroscience 2007;8():108-108.</p><p>Published online 19 Dec 2007</p><p>PMCID:PMC2211487.</p><p></p> eyes examined; control 11.8 ± 0.2, 19; Ag-treated 11.7 ± 0.2, 23; P = 0.76). Ag-treatment did not affect the ocular hypertension during the key window in disease progression, between 10 and 11 months (control, 18.2 ± 1.0, 31; Ag-treatment, 16.6 ± 1.3, 30; P = 0.334). () Ag-treatment from 5 months of age does not alter glaucomatous neurodegeneration (given as total number analyzed, treatment group, number of that treatment with mild, moderate, severe glaucoma) 10 months, 51 controls, 22,6,23; 51 Ag-treated 21,6,25; P = 0.293; 11.5 months, 55 controls, 18,6,31; 46 Ag-treated, 16,7,23, P = 0.896. (C) Ag-treatment beginning at 3 months of age does not protect from glaucomatous neurodegeneration. Nine months old treated mice actually tended to have more severe damage (given as total number analyzed, treatment group, number of that treatment with mild, moderate, severe glaucoma) 9 months, 42 controls, 27,7,8; 41 Ag-treated 17,6,18; P = 0.04; 10 months, 43 controls, 10,1,32; 49 Ag-treated, 6,2,41, P = 0.4; 11 months, 43 controls, 4,3,36; 37 Ag-treated, 5,3,29, P = 0.8. The experiments shown in B and C were performed at different institutions (see text)

Inducible nitric oxide synthase, , does not mediate optic neuropathy and retinopathy in the DBA/2J glaucoma model-4

<p><b>Copyright information:</b></p><p>Taken from "Inducible nitric oxide synthase, , does not mediate optic neuropathy and retinopathy in the DBA/2J glaucoma model"</p><p>http://www.biomedcentral.com/1471-2202/8/108</p><p>BMC Neuroscience 2007;8():108-108.</p><p>Published online 19 Dec 2007</p><p>PMCID:PMC2211487.</p><p></p>using ΔCT ratios (see Methods). 'Control' eyes from 4 months old DBA/2J mice were considered to be pre-glaucomatous and showed no axon damage. 'Sample' eyes from 10.5 months old DBA/2J mice were assessed for glaucomatous axon damage and grouped into the no or early, moderate or severe stages of damage (see Methods). Values given are relative to pre-glaucoma controls. expression was variable within each disease group (indicated by the SEM bars). Overall it decreased comparing pre-glaucoma with no or early glaucoma and increased modestly in eyes with moderate glaucoma (p < 0.05). () NOS2 protein localization in LPS-treated kidney (above) and no primary control (below). The NOS2 antibody shows strong and specific NOS2 staining (Red) in LPS-treated kidneys, with no non-specific binding of the secondary antibody. () NOS2 protein localization in the optic nerve heads of 10.5 months old DBA/2J mice, with the lower panels showing higher magnification of the boxed regions. There was no obvious correlation between NOS2 localization and glaucoma progression, although rare NOS2 positive cells were seen in eyes with severe glaucoma (arrow). All sections were processed, stained and imaged under identical conditions. The images shown here are representative of three different sections from three different eyes with the three different stages of glaucoma. Bars = 75 μm

Inducible nitric oxide synthase, , does not mediate optic neuropathy and retinopathy in the DBA/2J glaucoma model-1

<p><b>Copyright information:</b></p><p>Taken from "Inducible nitric oxide synthase, , does not mediate optic neuropathy and retinopathy in the DBA/2J glaucoma model"</p><p>http://www.biomedcentral.com/1471-2202/8/108</p><p>BMC Neuroscience 2007;8():108-108.</p><p>Published online 19 Dec 2007</p><p>PMCID:PMC2211487.</p><p></p>nd the bars show the extremes including outliers. The centerline of each diamond is the mean with the upper and lower points of each diamond representing the 95% confidence intervals of the mean. Mean ± s.e.m in mm Hg, number of eyes examined; 3.5 months, 12.6 ± 0.24, 18; 11.9 ± 0.30, 19; 12.2 ± 0.19, 19; P value for all comparisons > 0.08; 10–11 months, 21.9 ± 0.87, 39; 21.0 ± 0.95, 32; 23.6 ± 1.3, 30, P value for all comparisons >0.09

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

<p><b>Copyright information:</b></p><p>Taken from "Inducible nitric oxide synthase, , does not mediate optic neuropathy and retinopathy in the DBA/2J glaucoma model"</p><p>http://www.biomedcentral.com/1471-2202/8/108</p><p>BMC Neuroscience 2007;8():108-108.</p><p>Published online 19 Dec 2007</p><p>PMCID:PMC2211487.</p><p></p>s of DBA/2J mice develop severe optic nerve degeneration (). () The complete absence of NOS2 did not prevent glaucomatous neurodegeneration as many nerves had severe axonal damage. () genotype had no effect on the distribution of nerve damage. Numbers of nerves by age, genotype and disease state were: (given as total number analyzed, genotype, number of that genotype with mild, moderate, severe glaucoma) 3.5 months 6 6,0,0; 7 7,0,0;11 11,0,0; 10–12 months 53 23,3,27; 53 21,9,23; 56 17,3,36 (P value for all comparisons > 0.3). Average counts of RGC layer neurons from mice of each genotype with either severe glaucomatous damage or no detectable glaucomatous damage (total number of cells of the 8 fields counted per retina; see methods). genotype conferred no differential protective effect to RGCs in eyes with different degrees of axon loss. RGCs comprise 45–50% of cells in the RGC layer [71] and so almost all RGCs were lost in mice with severe axon loss independent of genotype. Percentage of surviving cells; , 54.4% ± 1.5; , 54.6% ± 1.5; , 58.0% ± 2.5; P values for all comparisons > 0.28. Number of retinal flat mounts counted, (given as genotype, mild, severe) 9, 7; 12, 8; 8, 13. Bar = 100 μm

Inducible nitric oxide synthase, , does not mediate optic neuropathy and retinopathy in the DBA/2J glaucoma model-0

<p><b>Copyright information:</b></p><p>Taken from "Inducible nitric oxide synthase, , does not mediate optic neuropathy and retinopathy in the DBA/2J glaucoma model"</p><p>http://www.biomedcentral.com/1471-2202/8/108</p><p>BMC Neuroscience 2007;8():108-108.</p><p>Published online 19 Dec 2007</p><p>PMCID:PMC2211487.</p><p></p>using ΔCT ratios (see Methods). 'Control' eyes from 4 months old DBA/2J mice were considered to be pre-glaucomatous and showed no axon damage. 'Sample' eyes from 10.5 months old DBA/2J mice were assessed for glaucomatous axon damage and grouped into the no or early, moderate or severe stages of damage (see Methods). Values given are relative to pre-glaucoma controls. expression was variable within each disease group (indicated by the SEM bars). Overall it decreased comparing pre-glaucoma with no or early glaucoma and increased modestly in eyes with moderate glaucoma (p < 0.05). () NOS2 protein localization in LPS-treated kidney (above) and no primary control (below). The NOS2 antibody shows strong and specific NOS2 staining (Red) in LPS-treated kidneys, with no non-specific binding of the secondary antibody. () NOS2 protein localization in the optic nerve heads of 10.5 months old DBA/2J mice, with the lower panels showing higher magnification of the boxed regions. There was no obvious correlation between NOS2 localization and glaucoma progression, although rare NOS2 positive cells were seen in eyes with severe glaucoma (arrow). All sections were processed, stained and imaged under identical conditions. The images shown here are representative of three different sections from three different eyes with the three different stages of glaucoma. Bars = 75 μm