Hydrogen Peroxide in Inflammation: Messenger, Guide, and Assassin

Wittmann, Christine; Chockley, Peter; Singh, Sachin Kumar; Pase, Luke; Lieschke, Graham J.; Grabher, Clemens

doi:10.1155/2012/541471

Cited by 108 publications

(86 citation statements)

References 40 publications

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“…This gradient, in fact, attracts immune cells toward the wound edges. In addition, a redox sensor has been identified in the leading edge of neutrophils (Wittmann et al, 2012;Yoo et al, 2011Yoo et al, , 2012 and topical application of low doses of H 2 O 2 enhances wound closure in mice (Loo et al, 2012). Importantly, ROS are required for the regeneration of planarian head and tail (Pirotte et al, 2015), zebrafish caudal fin (Gauron et al, 2013) and heart (Han et al, 2014), Xenopus tadpole tail (Love et al, 2013), and gecko tail (Zhang et al, 2016).…”

Section: Introductionmentioning

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: Introductionmentioning

confidence: 99%

Early bioelectric activities mediate redox-modulated regeneration

et al. 2016

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“…They are produced as natural byproducts of normal metabolism and play beneficial roles in cell signaling [40]. However, excessive ROS can be detrimental to cells as a result of induction of oxidative stress and cellular damage [41]. Earlier studies describing the chronic effect of glutamate exposure in cellular toxicity point to the crucial role of oxidative stress-induced ROS as a major stimulus of glutamate-induced cell death [17, 42–45].…”

Section: Discussionmentioning

confidence: 99%

Selenium suppresses glutamate-induced cell death and prevents mitochondrial morphological dynamic alterations in hippocampal HT22 neuronal cells

Ibeanu

Wang

et al. 2017

BMC Neurosci

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BackgroundPrevious studies have indicated that selenium supplementation may be beneficial in neuroprotection against glutamate-induced cell damage, in which mitochondrial dysfunction is considered a major pathogenic feature. However, the exact mechanisms by which selenium protects against glutamate-provoked mitochondrial perturbation remain ambiguous. In this study glutamate exposed murine hippocampal neuronal HT22 cell was used as a model to investigate the underlying mechanisms of selenium-dependent protection against mitochondria damage.ResultsWe find that glutamate-induced cytotoxicity was associated with enhancement of superoxide production, activation of caspase-9 and -3, increases of mitochondrial fission marker and mitochondrial morphological changes. Selenium significantly resolved the glutamate-induced mitochondria structural damage, alleviated oxidative stress, decreased Apaf-1, caspases-9 and -3 contents, and altered the autophagy process as observed by a decline in the ratio of the autophagy markers LC3-I and LC3-II.ConclusionThese findings suggest that the protection of selenium against glutamate stimulated cell damage of HT22 cells is associated with amelioration of mitochondrial dynamic imbalance.

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“…NF-κB factors are sensitive to redox state, and likely act downstream of early hydrogen peroxide signaling to stimulate inflammatory responses [77, 78]. The basic-Helix-loop-Helix transcription factor Hypoxia-inducible factor 1 alpha ( HIF-1α ) is expressed at many injury sites following blood vessel changes [76].…”

Section: Discussionmentioning

confidence: 99%

A distinct regulatory region of the Bmp5 locus activates gene expression following adult bone fracture or soft tissue injury

Guenther

Wang

et al. 2015

Bone

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Bone morphogenetic proteins (BMPs) are key signaling molecules required for normal development of bones and other tissues. Previous studies have shown that null mutations in the mouse Bmp5 gene alter the size, shape and number of multiple bone and cartilage structures during development. Bmp5 mutations also delay healing of rib fractures in adult mutants, suggesting that the same signals used to pattern embryonic bone and cartilage are also reused during skeletal regeneration and repair. Despite intense interest in BMPs as agents for stimulating bone formation in clinical applications, little is known about the regulatory elements that control developmental or injury-induced BMP expression. To compare the DNA sequences that activate gene expression during embryonic bone formation and following acute injuries in adult animals, we assayed regions surrounding the Bmp5 gene for their ability to stimulate lacZ reporter gene expression in transgenic mice. Multiple genomic fragments, distributed across the Bmp5 locus, collectively coordinate expression in discrete anatomic domains during normal development, including in embryonic ribs. In contrast, a distinct regulatory region activated expression following rib fracture in adult animals. The same injury control region triggered gene expression in mesenchymal cells following tibia fracture, in migrating keratinocytes following dorsal skin wounding, and in regenerating epithelial cells following lung injury. The Bmp5 gene thus contains an “injury response” control region that is distinct from embryonic enhancers, and that is activated by multiple types of injury in adult animals.

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Hydrogen Peroxide in Inflammation: Messenger, Guide, and Assassin

Cited by 108 publications

References 40 publications

Early bioelectric activities mediate redox-modulated regeneration

Early bioelectric activities mediate redox-modulated regeneration

Selenium suppresses glutamate-induced cell death and prevents mitochondrial morphological dynamic alterations in hippocampal HT22 neuronal cells

A distinct regulatory region of the Bmp5 locus activates gene expression following adult bone fracture or soft tissue injury

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