Calcium Flashes Orchestrate the Wound Inflammatory Response through DUOX Activation and Hydrogen Peroxide Release

Razzell, William; Evans, Iwan Robert; Martin, Paul; Wood, Will

doi:10.1016/j.cub.2013.01.058

Cited by 281 publications

(383 citation statements)

References 32 publications

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“…Another candidate is Ca 2+ signaling. Wounding induces fast Ca 2+ influx and Ca 2+ flashes in X. laevis oocytes and Drosophila embryo, respectively (Luxardi et al, 2014;Razzell et al, 2013). Importantly, those flashes activate a NADPH oxidase (Duox).…”

Section: Towards a Comprehensive Model Of Redox And Bioelectric Integmentioning

confidence: 99%

Early bioelectric activities mediate redox-modulated regeneration

et al. 2016

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Reactive oxygen species (ROS) and electric currents modulate regeneration; however, the interplay between biochemical and biophysical signals during regeneration remains poorly understood. We investigate the interactions between redox and bioelectric activities during tail regeneration in Xenopus laevis tadpoles. We show that inhibition of NADPH oxidase-mediated production of ROS, or scavenging or blocking their diffusion into cells, impairs regeneration and consistently regulates the dynamics of membrane potential, transepithelial potential (TEP) and electric current densities (J I ) during regeneration. Depletion of ROS mimics the altered TEP and J I observed in the non-regenerative refractory period. Short-term application of hydrogen peroxide (H 2 O 2 ) rescues (from depleted ROS) and induces (from the refractory period) regeneration, TEP increase and J I reversal. H 2 O 2 is therefore necessary for and sufficient to induce regeneration and to regulate TEP and J I . Epistasis assays show that voltage-gated Na + channels act downstream of H 2 O 2 to modulate regeneration. Altogether, these results suggest a novel mechanism for regeneration via redoxbioelectric orchestration.

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Section: Towards a Comprehensive Model Of Redox And Bioelectric Integmentioning

confidence: 99%

Early bioelectric activities mediate redox-modulated regeneration

et al. 2016

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“…Conversely, PI3K-mediated migration is crucial for haemocytes to sense a chemotactic gradient from a wound, but not for developmental migration 46,67 . Finally, hydrogen peroxide (H 2 O 2 ) has been identified as the earliest wound attractant in Drosophila embryos and zebrafish larvae 68 . We have shown that Drosophila haemocytes are recruited towards the basal regions where cell competition is taking place to remove apoptotic cells 10 .…”

Section: Discussionmentioning

confidence: 99%

Active JNK-dependent secretion of Drosophila Tyrosyl-tRNA synthetase by loser cells recruits haemocytes during cell competition

2015

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Cell competition is a process by which the slow dividing cells (losers) are recognized and eliminated from growing tissues. Loser cells are extruded from the epithelium and engulfed by the haemocytes, the Drosophila macrophages. However, how macrophages identify the dying loser cells is unclear. Here we show that apoptotic loser cells secrete Tyrosyl-tRNA synthetase (TyrRS), which is best known as a core component of the translational machinery. Secreted TyrRS is cleaved by matrix metalloproteinases generating MiniTyr and EMAP fragments. EMAP acts as a guiding cue for macrophage migration in the Drosophila larvae, as it attracts the haemocytes to the apoptotic loser cells. JNK signalling and Kish, a component of the secretory pathway, are autonomously required for the active secretion of TyrRS by the loser cells. Altogether, this mechanism guarantees effective removal of unfit cells from the growing tissue.

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“…Inversely, only a few studies have investigated the redox status and redox regulation of macrophage biology during tissue injury/ repair. In wound-healing models in zebrafish and Drosophila embryo, leukocyte recruitment depends on an H 2 O 2 signal gradient generated by DUOX activation (237,271).…”

Section: A Myeloid Cellsmentioning

confidence: 99%

Redox Control of Skeletal Muscle Regeneration

Moal

Pialoux

Juban

et al. 2017

Antioxidants & Redox Signaling

139

120

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Skeletal muscle shows high plasticity in response to external demand. Moreover, adult skeletal muscle is capable of complete regeneration after injury, due to the properties of muscle stem cells (MuSCs), the satellite cells, which follow a tightly regulated myogenic program to generate both new myofibers and new MuSCs for further needs. Although reactive oxygen species (ROS) and reactive nitrogen species (RNS) have long been associated with skeletal muscle physiology, their implication in the cell and molecular processes at work during muscle regeneration is more recent. This review focuses on redox regulation during skeletal muscle regeneration. An overview of the basics of ROS/RNS and antioxidant chemistry and biology occurring in skeletal muscle is first provided. Then, the comprehensive knowledge on redox regulation of MuSCs and their surrounding cell partners (macrophages, endothelial cells) during skeletal muscle regeneration is presented in normal muscle and in specific physiological (exercise-induced muscle damage, aging) and pathological (muscular dystrophies) contexts. Recent advances in the comprehension of these processes has led to the development of therapeutic assays using antioxidant supplementation, which result in inconsistent efficiency, underlying the need for new tools that are aimed at precisely deciphering and targeting ROS networks. This review should provide an overall insight of the redox regulation of skeletal muscle regeneration while highlighting the limits of the use of nonspecific antioxidants to improve muscle function. Antioxid. Redox Signal. 27, 276-310.

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Calcium Flashes Orchestrate the Wound Inflammatory Response through DUOX Activation and Hydrogen Peroxide Release

Cited by 281 publications

References 32 publications

Early bioelectric activities mediate redox-modulated regeneration

Early bioelectric activities mediate redox-modulated regeneration

Active JNK-dependent secretion of Drosophila Tyrosyl-tRNA synthetase by loser cells recruits haemocytes during cell competition

Redox Control of Skeletal Muscle Regeneration

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