Stress‐induced activation of Nox contributes to cell survival signalling via production of hydrogen peroxide

Groeger, Gillian; Mackey, Ashley; Pettigrew, Christopher A.; Bhatt, Lavinia; Cotter, Thomas G.

doi:10.1111/j.1471-4159.2009.06081.x

Cited by 53 publications

(40 citation statements)

References 58 publications

(122 reference statements)

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“…NADPH also helps to inhibit caspase-mediated apoptosis, support anabolic activity, and maintain appropriate levels of reactive oxygen species. 12,18,19,99 …”

Section: Glucose Metabolism In Photoreceptorsmentioning

confidence: 99%

Glucose metabolism in mammalian photoreceptor inner and outer segments

Narayan

Chidlow

Wood

et al. 2017

Clinical Exper Ophthalmology

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Photoreceptors are the first-order neurons of the visual pathway, converting light into electrical signals. Rods and cones are the two main types of photoreceptors in the mammalian retina. Rods are specialized for sensitivity at the expense of resolution and are responsible for vision in dimly lit conditions. Cones are responsible for high acuity central vision and colour vision. Many human retinal diseases are characterized by a progressive loss of photoreceptors. Photoreceptors consist of four primary regions: outer segments, inner segments, cell bodies and synaptic terminals. Photoreceptors consume large amounts of energy, and therefore, energy metabolism may be a critical juncture that links photoreceptor function and survival. Cones require more energy than rods, and cone degeneration is the main cause of clinically significant vision loss in retinal diseases. Photoreceptor segments are capable of utilizing various energy substrates, including glucose, to meet their large energy demands. The pathways by which photoreceptor segments meet their energy demands remain incompletely understood. Improvements in the understanding of glucose metabolism in photoreceptor segments may provide insight into the reasons why photoreceptors degenerate due to energy failure. This may, in turn, assist in developing bio-energetic therapies aimed at protecting photoreceptors.

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“…NADPH also helps to inhibit caspase-mediated apoptosis, support anabolic activity, and maintain appropriate levels of reactive oxygen species. 12,18,19,99 …”

Section: Glucose Metabolism In Photoreceptorsmentioning

confidence: 99%

Glucose metabolism in mammalian photoreceptor inner and outer segments

Narayan

Chidlow

Wood

et al. 2017

Clinical Exper Ophthalmology

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“…O-Linked protein glycosylation also is important as it plays a role in intracellular signaling (31,32). Glucose also is needed for production of cytosolic NADPH, which can inhibit caspase-mediated apoptosis (33,34), support anabolic activity (24,35), and help to maintain appropriate levels of reactive oxygen species (36). Finally, glucose deprivation activates autophagy (37), which has been described as a prosurvival activity (15,38,39).…”

Section: Degeneration Of Photoreceptor Neurons (Pr)mentioning

confidence: 99%

Roles of Glucose in Photoreceptor Survival

Chertov

Holzhausen

Kuok

et al. 2011

Journal of Biological Chemistry

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Background:The aim of this study is to understand the energy requirements of photoreceptor neurons. Results: Glucose withdrawal causes photoreceptor death. Mitochondrial fuels and autophagy can enhance survival. Conclusion: Mitochondrial activity and substrates for anabolic activity are required for photoreceptor survival. Significance: Understanding the energy requirements of photoreceptors will contribute to understanding the basis of retinal disease.

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“…Excessive H 2 O 2 exposure leads to oxidative stress and cell death, however low levels of H 2 O 2 can promote cell survival. 30 Therefore the role of H 2 O 2 in the survival of CD34 ϩ cells expressing H-Ras G12V was investigated (because this oncogene induced the strongest survival phenotype). CD34 ϩ H-Ras G12V cells showed a significant decrease in cell survival with decreasing cell culture density (P Ͻ .001; Figure 3B).…”

Section: Activated Ras Promotes Survival In Human Cd34 ؉ Cells But Ramentioning

confidence: 99%

mentioning

confidence: 99%

Ras-induced reactive oxygen species promote growth factor–independent proliferation in human CD34+ hematopoietic progenitor cells

Hole¹,

Pearn²,

Tonks

et al. 2010

Blood

112

108

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Excessive production of reactive oxygen species (ROS) is a feature of human malignancy and is often triggered by activation of oncogenes such as activated Ras. ROS act as second messengers and can influence a variety of cellular process including growth factor responses and cell survival. We have examined the contribution of ROS production to the effects of N-Ras G12D and H-Ras G12V on normal human CD34 ؉ progenitor cells. Activated Ras strongly up-regulated the production of both superoxide and hydrogen peroxide through the stimulation of NADPH oxidase (NOX) activity, without affecting the expression of endogenous antioxidants or the production of mitochondrially derived ROS. Activated Ras also promoted both the survival and the growth factor-independent proliferation of CD34 ؉ cells. Using oxidase inhibitors and antioxidants, we found that excessive ROS production by these cells did not contribute to their enhanced survival; rather, ROS promoted their growth factor-independent proliferation. Although Ras-induced ROS production specifically activated the p38 MAPK IntroductionReactive oxygen species (ROS) are a heterogeneous group of inorganic molecules and free radicals, with a wide spectrum of life span and reactivity. In physiologic systems, ROS formation begins with the univalent reduction of diatomic oxygen to produce superoxide radicals. There are 2 main sources of cellular superoxide; the first is the mitochondrial electron transport chain, where incomplete reduction of oxygen to water can result in superoxide formation. The other major source of superoxide is professional oxidases (exemplified by the NADPH oxidase [NOX] protein family), 1 which are expressed and functional throughout hematopoietic development. 2 These proteins form part of a membrane-bound complex that transfers single electrons from cytosolic nicotinamide adenine dinucleotide phosphate via flavin adenine dinucleotide to extracellular oxygen, producing superoxide. Superoxide is a shortlived radical but can dismutate forming hydrogen peroxide (H 2 O 2 ), a relatively long-lived species that lies at the hub of a variety of potential chemical reactions and is the main molecule from which all other physiologic ROS molecules are derived. ROS levels are regulated by a complex network of antioxidant molecules and enzymes that detoxify ROS. 3 For example, superoxide generation is balanced by the actions of superoxide dismutases (SODs), which convert superoxide to H 2 O 2 . Subsequently, H 2 O 2 is destroyed during oxidation reactions involving glutathione or members of the peroxiredoxin family.Although ROS production can have adverse consequences causing lipid peroxidation and DNA damage, it is also clear that ROS act as cell-signaling molecules. In recent years, it has become clear that H 2 O 2 reacts with a variety of proteins sensitive to thiol oxidation. 4 In particular, H 2 O 2 can inhibit phosphatases via oxidation of cysteine at the active site and may consolidate growth factor signaling by preventing futile cycles of phosphorylation a...

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Stress‐induced activation of Nox contributes to cell survival signalling via production of hydrogen peroxide

Cited by 53 publications

References 58 publications

Glucose metabolism in mammalian photoreceptor inner and outer segments

Glucose metabolism in mammalian photoreceptor inner and outer segments

Roles of Glucose in Photoreceptor Survival

Ras-induced reactive oxygen species promote growth factor–independent proliferation in human CD34+ hematopoietic progenitor cells

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