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Cited by 238Redox biology and oxidative stressMicrotubule and mitosis dynamicsCellular Mechanics and Interactions

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Regulation of cytoskeletal dynamics by redox signaling and oxidative stress: implications for neuronal development and trafficking

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Wilson, Carlos, González-Billault, Christian·2015·Frontiers in Cellular Neuroscience
DOI 10.3389/fncel.2015.00381PMC PMC4588006
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Abstract

A proper balance between chemical reduction and oxidation (known as redox balance) is essential for normal cellular physiology. Deregulation in the production of oxidative species leads to DNA damage, lipid peroxidation and aberrant post-translational modification of proteins, which in most cases induces injury, cell death and disease. However, physiological concentrations of oxidative species are necessary to support important cell functions, such as chemotaxis, hormone synthesis, immune response, cytoskeletal remodeling, Ca(2+) homeostasis and others. Recent evidence suggests that redox balance regulates actin and microtubule dynamics in both physiological and pathological contexts. Microtubules and actin microfilaments contain certain amino acid residues that are susceptible to oxidation, which reduces the ability of microtubules to polymerize and causes severing of actin microfilaments in neuronal and non-neuronal cells. In contrast, inhibited production of reactive oxygen species (ROS; e.g., due to NOXs) leads to aberrant actin polymerization, decreases neurite outgrowth and affects the normal development and polarization of neurons. In this review, we summarize emerging evidence suggesting that both general and specific enzymatic sources of redox species exert diverse effects on cytoskeletal dynamics. Considering the intimate relationship between cytoskeletal dynamics and trafficking, we also discuss the potential effects of redox balance on intracellular transport via regulation of the components of the microtubule and actin cytoskeleton as well as cytoskeleton-associated proteins, which may directly impact localization of proteins and vesicles across the soma, dendrites and axon of neurons.

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Figure 1 Regulation of the cytoskeleton dynamics by differential reactive oxygen species (ROS) levels. Physiological concentrations of ROS are needed for proper F-actin and microtubule dynamics both in vitro and in vivo. Oxidative stress induces the severing of F-actin and impairs microtubule polymerization. In the particular case of actin monomers, both Cys 374 and Met 42 residues are targets for oxidative molecules during oxidative stress conditions. Oxidation of Cys 374 leads to actin glutathionylation. On the other hand, oxidation of Met 44, which occurs specifically by MICAL1, leads to Met oxidation and severing of the actin filaments (Hung et al., 2011). Despite both α and β tubulin have several Cys residues that are susceptible to oxidation, it has not been described which Cys residues of tubulin monomers are modified by oxidation. In contrast, down-regulation of ROS synthesis, mainly through NOX inhibition, decreases the F-actin content and alters the dynamic properties of the actin cytoskeleton. None of the post-translational modification of actin monomers have been described after NOX inhibition and ROS down-regulation. Finally, the effect of the inhibition of ROS synthesis (below physiological levels) on microtubule dynamics has not been explored.
Figure 1 Regulation of the cytoskeleton dynamics by differential reactive oxygen species (ROS) levels. Physiological concentrations of ROS are needed for proper F-actin and microtubule dynamics both in vitro and in vivo. Oxidative stress induces the severing of F-actin and impairs microtubule polymerization. In the particular case of actin monomers, both Cys 374 and Met 42 residues are targets for oxidative molecules during oxidative stress conditions. Oxidation of Cys 374 leads to actin glutathionylation. On the other hand, oxidation of Met 44, which occurs specifically by MICAL1, leads to Met oxidation and severing of the actin filaments (Hung et al., 2011). Despite both α and β tubulin have several Cys residues that are susceptible to oxidation, it has not been described which Cys residues of tubulin monomers are modified by oxidation. In contrast, down-regulation of ROS synthesis, mainly through NOX inhibition, decreases the F-actin content and alters the dynamic properties of the actin cytoskeleton. None of the post-translational modification of actin monomers have been described after NOX inhibition and ROS down-regulation. Finally, the effect of the inhibition of ROS synthesis (below physiological levels) on microtubule dynamics has not been explored.CC BY · PubMed Central
Figure 2 Effect of physiological and non-physiological ROS on axonal growth cone organization. Oxidative stress (due to mitochondrial dysfunction, Sema3A/Plexin signaling and MICAL1 activation, neurodegenerative disorders, among others) induces the collapse of the axonal growth cones of neurons. In contrast, down-regulation of ROS synthesis, particularly due to NOX inhibition as well as Chronic Granulomatous Disease (CGD), decreases the F-actin content at the growth cone and affect filopodial dynamics by decreasing the number and length of filopodia at the axonal growth cone. Physiological concentrations of ROS, principally maintained by NOX enzymes and basal mitochondrial activity, are needed for a proper organization of the growth cones. In this context, the implicances for vesicular trafficking due to altered cytoskeleton dynamics has not been explored.
Figure 2 Effect of physiological and non-physiological ROS on axonal growth cone organization. Oxidative stress (due to mitochondrial dysfunction, Sema3A/Plexin signaling and MICAL1 activation, neurodegenerative disorders, among others) induces the collapse of the axonal growth cones of neurons. In contrast, down-regulation of ROS synthesis, particularly due to NOX inhibition as well as Chronic Granulomatous Disease (CGD), decreases the F-actin content at the growth cone and affect filopodial dynamics by decreasing the number and length of filopodia at the axonal growth cone. Physiological concentrations of ROS, principally maintained by NOX enzymes and basal mitochondrial activity, are needed for a proper organization of the growth cones. In this context, the implicances for vesicular trafficking due to altered cytoskeleton dynamics has not been explored.CC BY · PubMed Central

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Metadata

Authors
Wilson, C., & González-Billault, C.
Affiliations
University of Chile (CL)
Corresponding author
González-Billault, Christian
ORCID
Venue
Frontiers in Cellular Neuroscience
Publisher
Frontiers Media SA
Published
2015-09-30
Volume
9
Pages
381-381
ISSN
1662-5102 (ISSN-L)
DOI
10.3389/fncel.2015.00381
PMC
PMC4588006
OpenAlex
W1850305390
Cited by
238
References
103
Citations by year
2026: 23 · 2025: 19 · 2024: 12 · 2023: 14 · 2022: 32 · 2021: 32 · 2020: 35 · 2019: 22 · 2018: 16 · 2017: 14 · 2016: 16 · 2015: 2
FWCI
1.55
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • Frontiers in Cellular Neuroscience (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • Americanae (AECID Library) (submittedVersion, cc-by-nc-nd)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
  • LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (submittedVersion, cc-by-nc-nd)
  • Universidad de Chile (submittedVersion, cc-by-nc-nd)
Funders
  • Comisión Nacional de Investigación Científica y Tecnológica (ACT1114, 21120221)
  • Fondo Nacional de Desarrollo Científico y Tecnológico (1140325)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Microtubule and mitosis dynamics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular Mechanics and Interactions
Keywords
redox signaling, oxidative stress, redox homeostasis, cytoskeletal dynamics, actin dynamics, microtubule dynamics, reactive oxygen species, neuronal development, neuronal polarity, neurite outgrowth, intracellular trafficking, axonal transport, protein oxidation, nitric oxide synthase

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