scholarly journals Reactive oxygen species regulate activity-dependent neuronal plasticity in Drosophila

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Matthew CW Oswald ◽  
Paul S Brooks ◽  
Maarten F Zwart ◽  
Amrita Mukherjee ◽  
Ryan JH West ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Neuronal Plasticity ◽  
Second Messengers ◽  
Reactive Oxygen ◽  
Structural Plasticity ◽  
Oxygen Species ◽  
Redox Sensor ◽  
Motor Network ◽  
Network Output ◽  
Activity Dependent

Reactive oxygen species (ROS) have been extensively studied as damaging agents associated with ageing and neurodegenerative conditions. Their role in the nervous system under non-pathological conditions has remained poorly understood. Working with the Drosophila larval locomotor network, we show that in neurons ROS act as obligate signals required for neuronal activity-dependent structural plasticity, of both pre- and postsynaptic terminals. ROS signaling is also necessary for maintaining evoked synaptic transmission at the neuromuscular junction, and for activity-regulated homeostatic adjustment of motor network output, as measured by larval crawling behavior. We identified the highly conserved Parkinson’s disease-linked protein DJ-1β as a redox sensor in neurons where it regulates structural plasticity, in part via modulation of the PTEN-PI3Kinase pathway. This study provides a new conceptual framework of neuronal ROS as second messengers required for neuronal plasticity and for network tuning, whose dysregulation in the ageing brain and under neurodegenerative conditions may contribute to synaptic dysfunction.

scholarly journals Reactive Oxygen Species Regulate Activity-Dependent Neuronal Structural Plasticity in Drosophila

2016 ◽  
Author(s):  
Matthew C. W. Oswald ◽  
Paul S. Brooks ◽  
Maarten F. Zwart ◽  
Amrita Mukherjee ◽  
Ryan J. H. West ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Structural Changes ◽  
Second Messengers ◽  
Physiological Role ◽  
Reactive Oxygen ◽  
Structural Plasticity ◽  
Activity Level ◽  
Oxygen Species ◽  
Network Output ◽  
Activity Dependent

AbstractNeurons are inherently plastic, adjusting their structure, connectivity and excitability in response to changes in activity. How neurons sense changes in their activity level and then transduce these to structural changes remains to be fully elucidated. Working with the Drosophila larval locomotor network, we show that neurons use reactive oxygen species (ROS), metabolic byproducts, to monitor their activity. ROS signals are both necessary and sufficient for activity-dependent structural adjustments of both pre- and postsynaptic terminals and for network output, as measured by larval crawling behavior. We find the highly conserved Parkinson’s disease-linked protein DJ-1ß acts as a redox sensor in neurons where it regulates pre- and postsynaptic structural plasticity, in part via modulation of the PTEN-PI3Kinase pathway. Neuronal ROS thus play an important physiological role as second messengers required for neuronal and network tuning, whose dysregulation in the ageing brain and under neurodegenerative conditions may contribute to synaptic dysfunction.

scholarly journals Author response: Reactive oxygen species regulate activity-dependent neuronal plasticity in Drosophila

2018 ◽  
Author(s):  
Matthew CW Oswald ◽  
Paul S Brooks ◽  
Maarten F Zwart ◽  
Amrita Mukherjee ◽  
Ryan JH West ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Neuronal Plasticity ◽  
Reactive Oxygen ◽  
Author Response ◽  
Oxygen Species ◽  
Activity Dependent

scholarly journals Reactive Oxygen Species: Beyond Their Reactive Behavior

2021 ◽  
Vol 46 (1) ◽  
pp. 77-87
Author(s):  
Arnaud Tauffenberger ◽  
Pierre J. Magistretti
Keyword(s):  
Reactive Oxygen Species ◽  
Second Messengers ◽  
Critical Role ◽  
Complex Function ◽  
Reactive Oxygen ◽  
High Reactivity ◽  
Oxygen Species ◽  
Health And Disease ◽  
Cellular Dysfunction ◽  
The Brain

AbstractCellular homeostasis plays a critical role in how an organism will develop and age. Disruption of this fragile equilibrium is often associated with health degradation and ultimately, death. Reactive oxygen species (ROS) have been closely associated with health decline and neurological disorders, such as Alzheimer’s disease or Parkinson’s disease. ROS were first identified as by-products of the cellular activity, mainly mitochondrial respiration, and their high reactivity is linked to a disruption of macromolecules such as proteins, lipids and DNA. More recent research suggests more complex function of ROS, reaching far beyond the cellular dysfunction. ROS are active actors in most of the signaling cascades involved in cell development, proliferation and survival, constituting important second messengers. In the brain, their impact on neurons and astrocytes has been associated with synaptic plasticity and neuron survival. This review provides an overview of ROS function in cell signaling in the context of aging and degeneration in the brain and guarding the fragile balance between health and disease.

scholarly journals Reactive Oxygen Species in Venous Thrombosis

2020 ◽  
Vol 21 (6) ◽  
pp. 1918 ◽  
Author(s):  
Clemens Gutmann ◽  
Richard Siow ◽  
Adam M. Gwozdz ◽  
Prakash Saha ◽  
Alberto Smith
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Venous Thrombosis ◽  
Second Messengers ◽  
Redox Homeostasis ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Effector Cells ◽  
Systemic Oxidative Stress ◽  
The Complement System

Reactive oxygen species (ROS) have physiological roles as second messengers, but can also exert detrimental modifications on DNA, proteins and lipids if resulting from enhanced generation or reduced antioxidant defense (oxidative stress). Venous thrombus (DVT) formation and resolution are influenced by ROS through modulation of the coagulation, fibrinolysis, proteolysis and the complement system, as well as the regulation of effector cells such as platelets, endothelial cells, erythrocytes, neutrophils, mast cells, monocytes and fibroblasts. Many conditions that carry an elevated risk of venous thrombosis, such as the Antiphospholipid Syndrome, have alterations in their redox homeostasis. Dietary and pharmacological antioxidants can modulate several important processes involved in DVT formation, but their overall effect is unknown and there are no recommendations regarding their use. The development of novel antioxidant treatments that aim to abrogate the formation of DVT or promote its resolution will depend on the identification of targets that enable ROS modulation confined to their site of interest in order to prevent off-target effects on physiological redox mechanisms. Subgroups of patients with increased systemic oxidative stress might benefit from unspecific antioxidant treatment, but more clinical studies are needed to bring clarity to this issue.

scholarly journals A novel stress-inducible CmtR-ESX3-Zn2+ regulatory pathway essential for survival of Mycobacterium bovis under oxidative stress

2020 ◽  
Vol 295 (50) ◽  
pp. 17083-17099
Author(s):  
Xiaohui Li ◽  
Liu Chen ◽  
Jingjing Liao ◽  
Jiechen Hui ◽  
Weihui Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Mycobacterium Bovis ◽  
Reactive Oxygen ◽  
Negative Regulator ◽  
Oxygen Species ◽  
Bacterial Survival ◽  
Regulatory Pathway ◽  
Host Pathogen Interaction ◽  
Redox Sensor

Reactive oxygen species (ROS) are an unavoidable host environmental cue for intracellular pathogens such as Mycobacterium tuberculosis and Mycobacterium bovis; however, the signaling pathway in mycobacteria for sensing and responding to environmental stress remains largely unclear. Here, we characterize a novel CmtR-Zur-ESX3-Zn2+ regulatory pathway in M. bovis that aids mycobacterial survival under oxidative stress. We demonstrate that CmtR functions as a novel redox sensor and that its expression can be significantly induced under H2O2 stress. CmtR can physically interact with the negative regulator Zur and de-represses the expression of the esx-3 operon, which leads to Zn2+ accumulation and promotion of reactive oxygen species detoxication in mycobacterial cells. Zn2+ can also act as an effector molecule of the CmtR regulator, using which the latter can de-repress its own expression for further inducing bacterial antioxidant adaptation. Consistently, CmtR can induce the expression of EsxH, a component of esx-3 operon involved in Zn2+ transportation that has been reported earlier, and inhibit phagosome maturation in macrophages. Lastly, CmtR significantly contributes to bacterial survival in macrophages and in the lungs of infected mice. Our findings reveal the existence of an antioxidant regulatory pathway in mycobacteria and provide novel information on stress-triggered gene regulation and its association with host–pathogen interaction.

Redox signalling involving NADPH oxidase-derived reactive oxygen species

2006 ◽  
Vol 34 (5) ◽  
pp. 960-964 ◽  
Author(s):  
R. Dworakowski ◽  
N. Anilkumar ◽  
M. Zhang ◽  
A.M. Shah
Keyword(s):  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Second Messengers ◽  
Reactive Oxygen ◽  
Signalling Pathways ◽  
Cell Phenotype ◽  
Oxygen Species ◽  
Mechanical Stimuli ◽  
Nadph Oxidases ◽  
Redox Signalling

Increased oxidative stress plays an important role in the pathophysiology of many diseases such as atherosclerosis, diabetes mellitus, myocardial infarction and heart failure. In addition to the well-known damaging effects of oxygen-free radicals, ROS (reactive oxygen species) also have signalling roles, acting as second messengers that modulate the activity of diverse intracellular signalling pathways and transcription factors, thereby inducing changes in cell phenotype. NADPH oxidases appear to be especially important sources of ROS involved in redox signalling. Seven NADPH oxidase isoforms, known as Noxs (NAPDH oxidases), are expressed in a cell- and tissue-specific fashion. These oxidases are thought to subserve distinct functions as a result of their tightly regulated activation (e.g. by neurohormonal and growth factors and mechanical stimuli) and their specific coupling with distinct downstream signalling pathways. In the present paper, we review the structure and mechanisms of activation of NADPH oxidases and consider their involvement in redox signalling, focusing mainly on the cardiovascular system.

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