Glaucomatous outflow pathway and oxidative stress

Saccà, Sergio Claudio; Izzotti, Alberto; Rossi, P.; Traverso, Carlo Enrico

doi:10.1016/j.exer.2006.10.008

Cited by 223 publications

(184 citation statements)

References 97 publications

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“…28 -30 Several factors, including oxidative stress, 31 mitochondrial dysfunction, 32 and glutamate neurotoxicity 33,34 are proposed to work concomitantly in the pathogenesis of the disease and in regulating RGC susceptibility to glaucomatous damage. 35,36 Given possible involvement of NGB in these cellular functions, we hypothesized that NGB plays a role in glaucoma and may represent a novel target for treatment of the disease. Recently, we and others developed a convenient method of reproducibly inducing chronic IOP elevation in mice by anterior chamber injection of polystyrene microbeads.…”

mentioning

confidence: 99%

Neuroglobin Is an Endogenous Neuroprotectant for Retinal Ganglion Cells against Glaucomatous Damage

Wei

Cho

et al. 2011

The American Journal of Pathology

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Neuroglobin (NGB), a newly discovered member of the globin superfamily, may regulate neuronal survival under hypoxia or oxidative stress. Although NGB is greatly expressed in retinal neurons, the biological functions of NGB in retinal diseases remain largely unknown. We investigated the role of NGB in an experimental model of glaucoma, a neurodegenerative disorder that usually involves elevation of intraocular pressure (IOP). Elevated IOP is thought to induce oxidative stress in retinal ganglion cells (RGCs), thereby causing RGC death and, eventually, blindness. We found that NGB plays a critical role in increasing RGC resistance to ocular hypertension and glaucomatous damage. Neuroglobin (NGB) is a novel member of the globin superfamily that is distantly related to hemoglobin and myoglobin. 1 A highly conserved protein in evolution, human and mouse Ngb, both comprised of 151 amino acids, are 94% identical. 2,3 In mammals, expression of NGB is found in the brain, retina, and other nerve tissues, predominantly in neurons but absent from glial cells. 4 -7 Distribution of NGB protein in the normal human retina is very similar to what has been described in mice: NGB is detected primarily in the plexiform layers and photoreceptor inner segments, which are rich in mitochondria and synapses and consume high amounts of oxygen. 8,9 NGB has been shown to act as an endogenous neuroprotective molecule that enhances neuronal survival under hypoxic-ischemic insults in the brain 10 -12 ; however, its physiological functions and molecular mode of actions are not fully understood. Of note, NGB is present at a 100-fold greater concentration in the retina than in the brain, 8,[13][14][15] suggesting that the retina may be its most important site of function; however, among the many unknown roles of NGB, functional significance of NGB expression in the retina has been largely unexplored.

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mentioning

confidence: 99%

Neuroglobin Is an Endogenous Neuroprotectant for Retinal Ganglion Cells against Glaucomatous Damage

Wei

Cho

et al. 2011

The American Journal of Pathology

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“…These results pointed out that the continuous diffusion of serum selenium into aqueous humour leads to selenium overload within the MT cells. The increase of cellular selenium higher than the normal range could change the oxidant balance within the MT cells and may trigger the apoptotic signals (14). Coneley et al showed that the selenium overload within TM cells may affect outflow resistance, routine phagocytic function and extracellular matrix turnover (18).…”

Section: Discussionmentioning

confidence: 99%

“…Some studies have reported the association between serum selenium level and glaucoma (13) and have shown that selenium overload within aqueous humour may cause a decrease in trabecular meshwork cell adhesion and activation of apoptotic signaling pathways (14,15). Based on these reports, we evaluated the levels of selenium, selenoprotein P1 and some antioxidant parameters to test the hypothesis which suggests POAG may be related to a high selenium level.…”

Section: Introductionmentioning

confidence: 99%

Selenium and Selenoprotein P1 Levels Are Related to Primary Open-Angle Glaucoma / Nivoi Selena I Selenoproteina P1 Povezani Su Sa Primarnim Glaukomom Otvorenog Ugla

Najafi¹,

Yeganeh²,

Miraftabi³

et al. 2013

Journal of Medical Biochemistry

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SummaryBackground: Glaucoma is a highly prevalent eye disease related to optic nerve lesions and visual field defects. Primary Open-Angle Glaucoma (POAG) is a type of glaucoma that occurs frequently with unknown etiology. In this study, we investigated the serum levels of selenium, selenoprotein P1, glutathione, hemolysate glutathione peroxidase1 (GPx1) activity and aqueous humour selenium in POAG patients. Methods: Ninety sex-and age-matched subjects (POAG patients; n=45 and, controls; n=45) with the controlled confounders (smoking, hypertension and alcohol beverages) were recruited on clinical histories and exams. The serum and aqueous humour selenium levels were measured using GFAAS technique. The serum selenoprotein P1 level was assayed with the ELISA method. The hemolysate GPx1 activity and serum reduced glutathione level were also measured using known colorimetric techniques. Results: The serum selenium (P=0.01) and selenoprotein P1 (P<0.001) levels were significantly high in POAG patients. Furthermore, the aqueous humour selenium level was significantly high among patients as compared to controls (64.68±13.07 vs. 58.36±13.76 ng/mL, P=0.02). The results did not show a significant difference (P=0.36) in the hemolysate GPx1 activity between the groups. The cutoff points for intraocular pressure (IOP) and serum selenoprotein P1 parameters were estimated to be 39 mmHg (sensitivity 97.5%; 1-specificity 6.5%) and 188 mg/mL (sensitivity 93.5%; 1-specificity 14%), respectively.

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“…This mechanism of ischaemia-reperfusion injury is associated with the generation of reactive oxygen species and cellular apoptosis. These reactive oxygen species induce changes in the trabecular meshwork, possibly resulting in decreased aqueous humour drainage and increased IOP (Saccà, 2007). Additionally, they alter nitric oxide metabolism.…”

Section: Altered Blood Flow As a Risk Factor For Glaucoma (Progression)mentioning

confidence: 99%

A Vascular Approach to Glaucoma

Pinto¹,

Stalmans²

2011

Glaucoma - Basic and Clinical Concepts

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Glaucomatous outflow pathway and oxidative stress

Cited by 223 publications

References 97 publications

Neuroglobin Is an Endogenous Neuroprotectant for Retinal Ganglion Cells against Glaucomatous Damage

Neuroglobin Is an Endogenous Neuroprotectant for Retinal Ganglion Cells against Glaucomatous Damage

Selenium and Selenoprotein P1 Levels Are Related to Primary Open-Angle Glaucoma / Nivoi Selena I Selenoproteina P1 Povezani Su Sa Primarnim Glaukomom Otvorenog Ugla

A Vascular Approach to Glaucoma

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