2000
DOI: 10.1002/(sici)1098-1136(200004)30:2<178::aid-glia7>3.0.co;2-c
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Expression of nitric oxide synthase-2 (NOS-2) in reactive astrocytes of the human glaucomatous optic nerve head

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Cited by 165 publications
(89 citation statements)
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“…Oxidative injury due to amplified ROS generation (Levin, 1999), as well as nitric oxide-induced damage (Liu and Neufeld, 2000;Neufeld et al, 1999) has been suggested to be a part of the pathway for RGC death following axonal injury. Oxidative neuronal injury in glaucoma may also be associated with excitotoxic amino acids, including glutamate, which are known to induce ROS generation; and oxidative stress is a leading mechanism of glutamate neurotoxicity (Atlante et al, 2001).…”
Section: Proposed Pathogenic Mechanisms Of Glaucomatous Neurodegeneramentioning
confidence: 99%
See 1 more Smart Citation
“…Oxidative injury due to amplified ROS generation (Levin, 1999), as well as nitric oxide-induced damage (Liu and Neufeld, 2000;Neufeld et al, 1999) has been suggested to be a part of the pathway for RGC death following axonal injury. Oxidative neuronal injury in glaucoma may also be associated with excitotoxic amino acids, including glutamate, which are known to induce ROS generation; and oxidative stress is a leading mechanism of glutamate neurotoxicity (Atlante et al, 2001).…”
Section: Proposed Pathogenic Mechanisms Of Glaucomatous Neurodegeneramentioning
confidence: 99%
“…In vitro studies have revealed that in addition to TNF-α, exposure to glaucomatous stimuli also induces nitric oxide production by glial cells; and treatment of co-cultures with a selective inhibitor of inducible nitric oxide synthase, 1400W, results in a decreased rate of RGC death . Nitric oxide produced by glial cells has also been suggested to play a role in retrograde axonal degeneration and RGC death following axotomy (Koeberle and Ball, 1999) as well as IOP elevation (Liu and Neufeld, 2000;Neufeld et al, 1999).…”
Section: Oxidant Injury To Rgcsmentioning
confidence: 99%
“…We, and others, have found that reactive astrocytes are particularly active during optic nerve degeneration and are likely to contribute to the pathogenesis of glaucomatous optic neuropathy (Hernandez, 2000;Neufeld and Liu, 2003b). Screening the regulatory pathways of reactive astrocytes (Neufeld and Liu, 2003a), we demonstrated that the epidermal growth factor receptor (EGFR) pathway is an upstream signal of astrocytes in response to elevated hydrostatic pressure and causes optic nerve astrocytes to express inducible nitric oxide synthase and cyclooxygenase-2, to change shape, to increase levels of glial fibrillary acidic protein (GFAP), to modify the extracellular matrix, and to proliferate (Liu and Neufeld, 2000, 2004aZhang and Neufeld, 2005). All of these activities are characteristic of the reactive astrocyte phenotype.…”
Section: Introductionmentioning
confidence: 99%
“…25 Interestingly, in patients with glaucomatous optic neuropathy, levels of the enzymes cyclooxygenase-1 and nitric oxide synthase, which are involved in the synthesis of eicosanoids and nitric oxide, respectively, and are associated with retinal astrocytes, are elevated in glaucomatous eyes. 26,27 Likewise, in animal models of glaucoma, ganglion cell death is attenuated by treatment with inhibitors of astrocyteassociated nitric oxide synthase. 28 These data support the view that nitric oxide is one toxic factor that is released from astrocytes in glaucoma and damages ganglion cells.…”
Section: Introductionmentioning
confidence: 99%