Special Issue "NADPH Oxidase and Redox Signaling"

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (31 March 2021) | Viewed by 6203

Special Issue Editor

Dr. Ángel Hernández-Hernández
E-Mail Website
Guest Editor
Department of Biochemistry and Molecular Biology, University of Salamanca, Salamanca, Spain
Interests: NADPH oxidases; ROS; Redox signaling; hematopoiesis; leukemia; beta-catenin; PTPs

Special Issue Information

Dear Colleagues,

Traditionally reactive oxygen species (ROS) have been considered as detrimental for cell biology due to their capacity to oxidize proteins, lipids or nucleic acids. However, during the last two decades, we have become aware of the physiological importance of a moderate production of ROS. The concept of ROS as second messengers is currently widely accepted. In order to fully understand the importance of ROS for the control of cellular signaling, we would need to identify the signaling proteins regulated by ROS and also to understand how the production of ROS is regulated in physiological conditions. NADPH oxidases are a family of enzymes, present in all eukaryotic cells. Their only known function is the production of ROS; moreover, their activity can be regulated. In other words, this family of enzymes fulfils all the requirements for being one of the main sources of ROS involved in redox signaling. An interesting challenge is to unravel the specific role of the different NADPH oxidase family members for cell biology and physiology. This Special Issue aims to collect papers dealing with the role of NADPH oxidases in the regulation of cell function and physiology. Studies addressing signaling pathways or signaling proteins specifically regulated by NADPH oxidases will be also welcomed.

Dr. Ángel Hernández-Hernández
Guest Editor

Manuscript Submission Information

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Keywords

  • NADPH oxidase
  • NOX
  • Redox signaling
  • ROS
  • Signaling protein reversible oxidation

Published Papers (3 papers)

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Research

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Article
Effects of Iodonium Analogs on Nadph Oxidase 1 in Human Colon Cancer Cells
Antioxidants 2021, 10(11), 1757; https://doi.org/10.3390/antiox10111757 - 03 Nov 2021
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Abstract
Recent studies suggest that of the molecules postulated to function as inhibitors of the NADPH oxidase family of enzymes iodonium analogs known to broadly interfere with flavin dehydrogenase function demonstrate mechanistic validity as NADPH oxidase poisons. In recent work, we have produced a [...] Read more.
Recent studies suggest that of the molecules postulated to function as inhibitors of the NADPH oxidase family of enzymes iodonium analogs known to broadly interfere with flavin dehydrogenase function demonstrate mechanistic validity as NADPH oxidase poisons. In recent work, we have produced a series of novel iodonium compounds as putative inhibitors of these oxidases. To evaluate the potential utility of two novel molecules with favorable chemical properties, NSC 740104 and NSC 751140, we compared effects of these compounds to the two standard inhibitors of this class, diphenyleneiodonium and di-2-thienyliodonium, with respect to antiproliferative, cell cycle, and gene expression effects in human colon cancer cells that require the function of NADPH oxidase 1. Both new agents blocked NADPH oxidase-related reactive oxygen production, inhibited tumor cell proliferation, produced a G1/S block in cell cycle progression, and inhibited NADPH oxidase 1 expression at the mRNA and protein levels at low nM concentrations in a fashion similar to or better than the parent molecules. These studies suggest that NSC 740104 and NSC 751140 should be developed further as mechanistic tools to better understand the role of NADPH oxidase inhibition as an approach to the development of novel therapeutic agents for colon cancer. Full article
(This article belongs to the Special Issue NADPH Oxidase and Redox Signaling)
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Article
Immunological Aspects of X-Linked Chronic Granulomatous Disease Female Carriers
Antioxidants 2021, 10(6), 891; https://doi.org/10.3390/antiox10060891 - 01 Jun 2021
Cited by 1 | Viewed by 1264
Abstract
X-linked Granulomatous Disease (XL-CGD) carriers were previously thought to be clinically healthy because random X-chromosome inactivation (XCI) allows approximately half of their phagocytes/monocytes to express functional gp91phox protein. This supports the NADPH oxidase activity necessary for the killing of engulfed pathogens. Some XL-CGD [...] Read more.
X-linked Granulomatous Disease (XL-CGD) carriers were previously thought to be clinically healthy because random X-chromosome inactivation (XCI) allows approximately half of their phagocytes/monocytes to express functional gp91phox protein. This supports the NADPH oxidase activity necessary for the killing of engulfed pathogens. Some XL-CGD carriers suffer from inflammatory and autoimmune manifestations as well as infections, although the skewed-XCI of a mutated allele is reported to be exclusively determinant for infection susceptibility. Indeed, immune dysregulation could be determined by dysfunctional non-phagocytic leukocytes rather than the percentage of functioning neutrophils. Here we investigated in a cohort of 12 X-CGD female carriers at a particular time of their life the gp91phox protein expression/function and how this affects immune cell function. We showed that 50% of carriers have an age-independent skewed-XCI and 65% of them have a misrepresented expression of the wild-type gene. The majority of carriers manifested immune dysregulation and GI manifestations regardless of age and XCI. Immunological investigations revealed an increase in CD19+ B cells, CD56bright-NK cell percentage, a slightly altered CD107a upregulation on CD4+ T cells, and reduced INFγ-production by CD4+ and CD8+ cells. Notably, we demonstrated that the residual level of ROS robustly correlates with INFγ-expressing T cells, suggesting a role in promoting immune dysregulation in carriers. Full article
(This article belongs to the Special Issue NADPH Oxidase and Redox Signaling)
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Review

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Review
NADPH Oxidases (NOX): An Overview from Discovery, Molecular Mechanisms to Physiology and Pathology
Antioxidants 2021, 10(6), 890; https://doi.org/10.3390/antiox10060890 - 01 Jun 2021
Cited by 49 | Viewed by 3974
Abstract
The reactive oxygen species (ROS)-producing enzyme NADPH oxidase (NOX) was first identified in the membrane of phagocytic cells. For many years, its only known role was in immune defense, where its ROS production leads to the destruction of pathogens by the immune cells. [...] Read more.
The reactive oxygen species (ROS)-producing enzyme NADPH oxidase (NOX) was first identified in the membrane of phagocytic cells. For many years, its only known role was in immune defense, where its ROS production leads to the destruction of pathogens by the immune cells. NOX from phagocytes catalyzes, via one-electron trans-membrane transfer to molecular oxygen, the production of the superoxide anion. Over the years, six human homologs of the catalytic subunit of the phagocyte NADPH oxidase were found: NOX1, NOX3, NOX4, NOX5, DUOX1, and DUOX2. Together with the NOX2/gp91phox component present in the phagocyte NADPH oxidase assembly itself, the homologs are now referred to as the NOX family of NADPH oxidases. NOX are complex multidomain proteins with varying requirements for assembly with combinations of other proteins for activity. The recent structural insights acquired on both prokaryotic and eukaryotic NOX open new perspectives for the understanding of the molecular mechanisms inherent to NOX regulation and ROS production (superoxide or hydrogen peroxide). This new structural information will certainly inform new investigations of human disease. As specialized ROS producers, NOX enzymes participate in numerous crucial physiological processes, including host defense, the post-translational processing of proteins, cellular signaling, regulation of gene expression, and cell differentiation. These diversities of physiological context will be discussed in this review. We also discuss NOX misregulation, which can contribute to a wide range of severe pathologies, such as atherosclerosis, hypertension, diabetic nephropathy, lung fibrosis, cancer, or neurodegenerative diseases, giving this family of membrane proteins a strong therapeutic interest. Full article
(This article belongs to the Special Issue NADPH Oxidase and Redox Signaling)
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