Redox regulation of cytoskeletal dynamics during differentiation and de-differentiation

Gellert, Manuela; Hanschmann, Eva-Maria; Lepka, Klaudia; Berndt, Carsten; Lillig, Christopher Horst

doi:10.1016/j.bbagen.2014.10.030

Cited by 31 publications

(21 citation statements)

References 195 publications

(254 reference statements)

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“…Although oxidation inhibits F-actin polymerization, oxidation of cysteine residues activates the GTPase RhoA (37, 40, 41). Further, RhoA activation upon plasma membrane injury is required for F-actin buildup (42).…”

Section: Resultsmentioning

confidence: 99%

Mitochondrial redox signaling enables repair of injured skeletal muscle cells

et al. 2017

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Strain and physical trauma to mechanically active cells, such as skeletal muscle myofibers, injures their plasma membranes, and mitochondrial function is required for their repair. Here we found that mitochondrial function was also needed for plasma membrane repair in myoblasts as well as nonmuscle cells, which depended on mitochondrial uptake of calcium through the mitochondrial calcium uniporter (MCU). Calcium uptake transiently increased the production of mitochondrial reactive oxygen species (ROS), which locally activated the GTPase RhoA, triggering F-actin accumulation at the site of injury and facilitating membrane repair. Blocking mitochondrial calcium uptake or ROS production prevented injury-triggered RhoA activation, actin polymerization, and plasma membrane repair. This repair mechanism was shared between myoblasts, nonmuscle cells, and mature skeletal myofibers. Quenching mitochondrial ROS in myofibers during eccentric exercise ex vivo caused increased damage to myofibers, resulting in a greater loss of muscle force. These results suggest a physiological role for mitochondria in plasma membrane repair in injured cells, a role that highlights a beneficial effect of ROS.

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Section: Resultsmentioning

confidence: 99%

Mitochondrial redox signaling enables repair of injured skeletal muscle cells

et al. 2017

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“…Many of the redox-regulated proteins fall into the category of kinases, phosphatases, and transcription factors. However, there are also other types of proteins whose activity has been shown to be redox regulated, such as proteins involved in the cytoskeleton dynamics such as actin, tubulins, cofilin, semaphorins (125), GTPases (146,184), protein quality control proteins (40, 389), or dehydrogenases such as GAPDH (282).…”

Section: Mammalian Redox-regulated Proteinsmentioning

confidence: 99%

The Emerging Roles of Nicotinamide Adenine Dinucleotide Phosphate Oxidase 2 in Skeletal Muscle Redox Signaling and Metabolism

Henríquez‐Olguín

Boronat

Cabello-Verrugio

et al. 2019

Antioxidants & Redox Signaling

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Significance: Skeletal muscle is a crucial tissue to whole-body locomotion and metabolic health. Reactive oxygen species (ROS) have emerged as intracellular messengers participating in both physiological and pathological adaptations in skeletal muscle. A complex interplay between ROS-producing enzymes and antioxidant networks exists in different subcellular compartments of mature skeletal muscle. Recent evidence suggests that nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (NOXs) are a major source of contraction-and insulin-stimulated oxidants production, but they may paradoxically also contribute to muscle insulin resistance and atrophy. Recent Advances: Pharmacological and molecular biological tools, including redox-sensitive probes and transgenic mouse models, have generated novel insights into compartmentalized redox signaling and suggested that NOX2 contributes to redox control of skeletal muscle metabolism. Critical Issues: Major outstanding questions in skeletal muscle include where NOX2 activation occurs under different conditions in health and disease, how NOX2 activation is regulated, how superoxide/hydrogen peroxide generated by NOX2 reaches the cytosol, what the signaling mediators are downstream of NOX2, and the role of NOX2 for different physiological and pathophysiological processes. Future Directions: Future research should utilize and expand the current redox-signaling toolbox to clarify the NOX2-dependent mechanisms in skeletal muscle and determine whether the proposed functions of NOX2 in cells and animal models are conserved into humans.

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“…Besides these obvious points of potential redox regulation, it is now recognized that autophagy is controlled by cellular positioning of Rhebs, TSC1/2, mTORCs and lysosomes with respect to one another (Groenewood and Zwartkruis, 2010; Menon et al, 2014; Sancak et al, 2010;). Because protein trafficking is sensitive to both cytoskeletal integrity and redox-regulated PTMs of trafficking proteins (Gellert et al, 2014), this is another important possible point at which oxidative stress could compromise normal autophagy function. The remainder of this review will focus on evidence that autophagy is indeed dysfunctional in a variety of human neuropathologies, and evidence that this disruption may be due, in part, to dys homeostasis of specific redox mechanisms that might control or at least modulate the pace of neural autophagy.…”

Section: The Mechanics Of Autophagymentioning

confidence: 99%

Redox regulation of autophagy in healthy brain and neurodegeneration

Hensley

Harris-White

2015

Neurobiology of Disease

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Autophagy and redox biochemistry are two major sub disciplines of cell biology which are both coming to be appreciated for their paramount importance in the etiology of neurodegenerative diseases including Alzheimer’s disease (AD). Thus far, however, there has been relatively little exploration of the interface between autophagy and redox biology. Autophagy normally recycles macro-molecular aggregates produced through oxidative-stress mediated pathways, and also may reduce the mitochondrial production of reactive oxygen species through recycling of old and damaged mitochondria. Conversely, dysfunction in autophagy initiation, progression or clearance is evidenced to increase aggregation-prone proteins in neural and extraneural tissues. Redox mechanisms of autophagy regulation have been documented at the level of cross-talk between the Nrf2/Keap1 oxidant and electrophilic defense pathway and p62/sequestosome-1 (SQSTM1)-associated autophagy, at least in extraneural tissue; but other mechanisms of redox autophagy regulation doubtless remain to be discovered and the relevance of such processes to maintenance of neural homeostasis remain to be determined. This review summarizes current knowledge regarding the relationship of redox signaling, autophagy control, and oxidative stress as these phenomena relate to neurodegenerative disease. AD is specifically addressed as an example of the theme and as a promising indication for new therapies that act through engagement of autophagy pathways. To exemplify one such novel therapeutic entity, data is presented that the antioxidant and neurotrophic agent lanthionine ketimine-ethyl ester (LKE) affects autophagy pathway proteins including beclin-1 in the 3xTg-AD model of Alzheimer’s disease where the compound has been shown to reduce pathological features and cognitive dysfunction.

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Redox regulation of cytoskeletal dynamics during differentiation and de-differentiation

Cited by 31 publications

References 195 publications

Mitochondrial redox signaling enables repair of injured skeletal muscle cells

Mitochondrial redox signaling enables repair of injured skeletal muscle cells

The Emerging Roles of Nicotinamide Adenine Dinucleotide Phosphate Oxidase 2 in Skeletal Muscle Redox Signaling and Metabolism

Redox regulation of autophagy in healthy brain and neurodegeneration

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