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Role of NADPH Oxidase on Neuron Death or on Neurogenesis

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (31 March 2019) | Viewed by 25877

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Special Issue Editor

Prof. Dr. Sang Won Suh

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Guest Editor

Department of Physiology, College of Medicine, Hallym University, Chuncheon 24252, Republic of Korea
Interests: the pathogenic mechanisms of NADPH oxidase activation on neuronal death; the role of zinc in the brain; neurogenesis after ischemia, hypoglycemia, epilepsy and brain trauma; role of zinc on multiple sclerosis pathogenesis; Alzheimer's disease; NADPH oxidase; stroke

Special Issue Information

Dear Colleagues,

NADPH oxidase (nicotinamide adenine dinucleotide phosphate-oxidase) is present in many cell types, including neurons. NADPH oxidase is a multi-component enzyme, comprising a plasma membrane-bound subunit, gp91; a membrane-associated flavocytochrome, cytochrome b558; and at least three cytosolic subunits, p47^phox, p67^phox and the small G protein Rac2. During activation, the p47^phox component is phosphorylated and translocates to the plasma membrane, where it associates with the other subunits to form the active enzyme complex. Interestingly, previous studies examining the production of reactive oxygen species (ROS) in the brain during ischemia, traumatic brain injury and hypoglycemic insult suggest that superoxide is formed primarily during the reperfusion period. NADPH oxidase activation-induced superoxide production also has been suggested in the multiple sclerosis. However, the mechanism by which NADPH oxidase is activated in non-phagocytic cells is still not well understood.

Elevated levels of ROS can mediate deleterious neuronal effects, including neuronal toxicity and degeneration observed in the etiology of a many pathological conditions. However, ROS can modulate the redox state of tyrosine phosphorylated proteins, thereby having an impact on many transcriptional pathways and signaling cascades important for neurogenesis.

We invite you to contribute original articles that describe the role of NADPH oxidase on neuron degeneration or on neurogenesis. Review articles describing our current knowledge on any aspect ragarding NADPH oxidse activation-induced neuron death or neurogenesis are also welcome.

Although this Special Issue mainly concerns neurological aspects, we welcome all biological topics regarding NADPH oxidase activation.

Prof. Sang Won Suh
Guest Editor

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Keywords

NADPH oxidase
Neuron death
Neurogenesis
Zinc
Oxidative stress
Stroke
Epilepsy
Traumatic brain injury
Hypoglycemia
Neurodegenerative disease
Multiple sclerosis
Immunology
Development
Infection
And other biological topics

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Published Papers (4 papers)

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Research

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19 pages, 58648 KiB

Open AccessArticle

The Role of NOX4 in Parkinson’s Disease with Dementia

by Dong-Hee Choi, In-Ae Choi, Cheol Soon Lee, Ji Hee Yun and Jongmin Lee

Int. J. Mol. Sci. 2019, 20(3), 696; https://doi.org/10.3390/ijms20030696 - 6 Feb 2019

Cited by 17 | Viewed by 3999

Abstract

The neuropathology of Parkinson’s disease with dementia (PDD) has been reported to involve heterogeneous and various disease mechanisms. Alpha-synuclein (α-syn) and amyloid beta (Aβ) pathology are associated with the cognitive status of PDD, and NADPH oxidase (NOX) is known to affect a variety of cognitive functions. We investigated the effects of NOX on cognitive impairment and on α-syn and Aβ expression and aggregation in PDD. In the 6-hydroxydopamine (6-OHDA)-injected mouse model, cognitive and motor function, and the levels of α-syn, Aβ, and oligomer A11 after inhibition of NOX4 expression in the hippocampal dentate gyrus (DG) were measured by the Morris water maze, novel object recognition, rotation, and rotarod tests, as well as immunoblotting and immunohistochemistry. After 6-OHDA administration, the death of nigrostriatal dopamine neurons and the expression of α-syn and NOX1 in the substantia nigra were increased, and phosphorylated α-syn, Aβ, oligomer A11, and NOX4 were upregulated in the hippocampus. 6-OHDA dose-dependent cognitive impairment was observed, and the increased cognitive impairment, Aβ expression, and oligomer A11 production in 6-OHDA-treated mice were suppressed by NOX4 knockdown in the hippocampal DG. Our results suggest that increased expression of NOX4 in the hippocampal DG in the 6-OHDA-treated mouse induces Aβ expression and oligomer A11 production, thereby reducing cognitive function. Full article

(This article belongs to the Special Issue Role of NADPH Oxidase on Neuron Death or on Neurogenesis)

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12 pages, 2576 KiB

Open AccessArticle

Effect of Pretreatment with the NADPH Oxidase Inhibitor Apocynin on the Therapeutic Efficacy of Human Placenta-Derived Mesenchymal Stem Cells in Intracerebral Hemorrhage

by Saehong Min, Ok Joon Kim, Jinkun Bae and Tae Nyoung Chung

Int. J. Mol. Sci. 2018, 19(11), 3679; https://doi.org/10.3390/ijms19113679 - 21 Nov 2018

Cited by 18 | Viewed by 4909

Abstract

Several studies have demonstrated the beneficial effect of mesenchymal stem cells (MSCs) on intracerebral hemorrhage (ICH). Enhancement of the therapeutic efficacy of MSCs in ICH is necessary, considering the diseases high association with mortality and morbidity. Various preconditioning methods to enhance the beneficial properties of MSCs have been introduced. We suggested apocynin, a well-known nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitor, as a novel preconditioning regimen to enhance the therapeutic efficacy of MSCs in ICH. Rat ICH models were made using bacterial collagenase. 24 h after ICH induction, the rats were randomly divided into apocynin-preconditioned MSC-treated (Apo-MSC), naïve MSC-treated and control groups. Hematoma volume, brain edema, and degenerating neuron count were compared at 48 h after the ICH induction. The expression of tight junction proteins (occludin, zona occludens [ZO]-1) were also compared. Hematoma size, hemispheric enlargement and degenerating neuron count were significantly lower in the Apo-MSC group than in the naïve MSC group (p = 0.004, 0.013 and 0.043, respectively), while the expression of occludin was higher (p = 0.024). Apocynin treatment enhances the therapeutic efficacy of MSCs in ICH in the acute stage, through the improvement of the beneficial properties of MSCs, such as neuroprotection and the reinforcement of endovascular integrity of cerebral vasculature. Full article

(This article belongs to the Special Issue Role of NADPH Oxidase on Neuron Death or on Neurogenesis)

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15 pages, 1936 KiB

Open AccessArticle

Inhibition of NADPH Oxidase Activation by Apocynin Rescues Seizure-Induced Reduction of Adult Hippocampal Neurogenesis

by Song Hee Lee, Bo Young Choi, A Ra Kho, Jeong Hyun Jeong, Dae Ki Hong, Dong Hyeon Kang, Beom Seok Kang, Hong Ki Song, Hui Chul Choi and Sang Won Suh

Int. J. Mol. Sci. 2018, 19(10), 3087; https://doi.org/10.3390/ijms19103087 - 9 Oct 2018

Cited by 31 | Viewed by 4437

Abstract

Apocynin, also known as acetovanillone, is a natural organic compound structurally related to vanillin. Apocynin is known to be an inhibitor of NADPH (Nicotinamide adenine dinucleotide phosphate) oxidase activity and is highly effective in suppressing the production of superoxide. The neuroprotective effects of apocynin have been investigated in numerous brain injury settings, such as stroke, traumatic brain injury (TBI), and epilepsy. Our lab has demonstrated that TBI or seizure-induced oxidative injury and neuronal death were reduced by apocynin treatment. Several studies have also demonstrated that neuroblast production is transiently increased in the hippocampus after seizures. Here, we provide evidence confirming the hypothesis that long-term treatment with apocynin may enhance newly generated hippocampal neuronal survival by reduction of superoxide production after seizures. A seizure was induced by pilocarpine [(25 mg/kg intraperitoneal (i.p.)] injection. Apocynin was continuously injected for 4 weeks after seizures (once per day) into the intraperitoneal space. We evaluated neuronal nuclear antigen (NeuN), bromodeoxyuridine (BrdU), and doublecortin (DCX) immunostaining to determine whether treatment with apocynin increased neuronal survival and neurogenesis in the hippocampus after seizures. The present study indicates that long-term treatment of apocynin increased the number of NeuN⁺ and DCX⁺ cells in the hippocampus after seizures. Therefore, this study suggests that apocynin treatment increased neuronal survival and neuroblast production by reduction of hippocampal oxidative injury after seizures. Full article

(This article belongs to the Special Issue Role of NADPH Oxidase on Neuron Death or on Neurogenesis)

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Review

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19 pages, 772 KiB

Open AccessReview

The Role of NADPH Oxidases and Oxidative Stress in Neurodegenerative Disorders

by Anuradha Tarafdar and Giordano Pula

Int. J. Mol. Sci. 2018, 19(12), 3824; https://doi.org/10.3390/ijms19123824 - 30 Nov 2018

Cited by 264 | Viewed by 11918

Abstract

For a number of years, nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (NOX) was synonymous with NOX2/gp91^phox and was considered to be a peculiarity of professional phagocytic cells. Over the last decade, several more homologs have been identified and based on current research, the NOX family consists of NOX1, NOX2, NOX3, NOX4, NOX5, DUOX1 and DUOX2 enzymes. NOXs are electron transporting membrane proteins that are responsible for reactive oxygen species (ROS) generation—primarily superoxide anion (O₂^●−), although hydrogen peroxide (H₂O₂) can also be generated. Elevated ROS leads to oxidative stress (OS), which has been associated with a myriad of inflammatory and degenerative pathologies. Interestingly, OS is also the commonality in the pathophysiology of neurodegenerative disorders, such as Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD), amyotrophic lateral sclerosis (ALS) and multiple sclerosis (MS). NOX enzymes are expressed in neurons, glial cells and cerebrovascular endothelial cells. NOX-mediated OS is identified as one of the main causes of cerebrovascular damage in neurodegenerative diseases. In this review, we will discuss recent developments in our understanding of the mechanisms linking NOX activity, OS and neurodegenerative diseases, with particular focus on the neurovascular component of these conditions. We conclude highlighting current challenges and future opportunities to combat age-related neurodegenerative disorders by targeting NOXs. Full article

(This article belongs to the Special Issue Role of NADPH Oxidase on Neuron Death or on Neurogenesis)

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