Peroxiredoxin 3 has a crucial role in the contractile function of skeletal muscle by regulating mitochondrial homeostasis

Lee, Kwang-Pyo; Shin, Yeo Jin; Cho, Sung Chun; Lee, Seung Min; Bahn, Young Jae; Kim, Ji Young; Kwon, Eunjung; Jeong, Do Yeun; Park, Sang Chul; Rhee, Sue Goo; Woo, Hyun Ae; Kwon, Kideok D.

doi:10.1016/j.freeradbiomed.2014.09.010

Cited by 45 publications

(33 citation statements)

References 39 publications

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“…Table 2), and included a number of heat stress proteins and chaperones, which are normally induced in response to the accumulation of unfolded proteins formed under different stress conditions (62). Overall, it seems that Prx3 plays a defining role in mitochondrial functioning, and this notion is supported by studies conducted in mammals (63,64). Nevertheless, there is a considerable degree of redundancy with Prx5, based on the overlap of gene expression patterns of the single mutants and the additive nature of transcript levels in the DM (Fig.…”

Section: Discussionmentioning

confidence: 68%

Mitochondrial peroxiredoxins are essential in regulating the relationship between Drosophila immunity and aging

Odnokoz

Nakatsuka

Klichko

et al. 2017

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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Previously, we have shown that flies under-expressing the two mitochondrial peroxiredoxins (Prxs), dPrx3 and dPrx5, display increases in tissue-specific apoptosis and dramatically shortened life span, associated with a redox crisis, manifested as changes in GSH:GSSG and accumulation of protein mixed disulfides. To identify specific pathways responsible for the observed biological effects, we performed a transcriptome analysis. Functional clustering revealed a prominent group enriched for immunity-related genes, including a considerable number of NF-kB-dependent antimicrobial peptides (AMP) that are up-regulated in the Prx double mutant. Using qRT-PCR analysis we determined that the age-dependent changes in AMP levels in mutant flies were similar to those observed in controls when scaled to percentage of life span. To further clarify the role of Prx-dependent mitochondrial signaling, we expressed different forms of dPrx5, which unlike the uniquely mitochondrial dPrx3 is found in multiple subcellular compartments, including mitochondrion, nucleus and cytosol. Ectopic expression of dPrx5 in mitochondria but not nucleus or cytosol partially extended longevity under normal or oxidative stress conditions while complete restoration of life span occurred when all three forms of dPrx5 were expressed from the wild type dPrx5 transgene. When dPrx5 was expressed in mitochondria or in all three compartments, it substantially delayed the development of hyperactive immunity while expression of cytosolic or nuclear forms had no effect on the immune phenotype. The data suggest a critical role of mitochondria in development of chronic activation of the immune response triggered by impaired redox control.

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Section: Discussionmentioning

confidence: 68%

Mitochondrial peroxiredoxins are essential in regulating the relationship between Drosophila immunity and aging

Odnokoz

Nakatsuka

Klichko

et al. 2017

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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“…Free radical processes increasing is the main pathogenic factor during skeletal muscles fatigue development [58]. Under significant physical activity there is highly overproduction of free radicals in muscle tissue that intensifies the processes of lipid peroxidation, cell membranes damage and antioxidant enzymes inactivation [59].…”

Section: Discussionmentioning

confidence: 99%

C60 fullerene as promising therapeutic agent for correcting and preventing skeletal muscle fatigue

et al. 2017

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BackgroundBioactive soluble carbon nanostructures, such as the C60 fullerene can bond with up to six electrons, thus serving by a powerful scavenger of reactive oxygen species similarly to many natural antioxidants, widely used to decrease the muscle fatigue effects. The aim of the study is to define action of the pristine C60 fullerene aqueous colloid solution (C60FAS), on the post-fatigue recovering of m. triceps surae in anaesthetized rats.ResultsDuring fatigue development, we observed decrease in the muscle effort level before C60FAS administration. After the application of C60FAS, a slower effort decrease, followed by the prolonged retention of a certain level, was recorded. An analysis of the metabolic process changes accompanying muscle fatigue showed an increase in the oxidative stress markers H 2 O 2 (hydrogen peroxide) and TBARS (thiobarbituric acid reactive substances) in relation to the intact muscles. After C60FAS administration, the TBARS content and H 2 O 2 level were decreased. The endogenous antioxidant system demonstrated a similar effect because the GSH (reduced glutathione) in the muscles and the CAT (catalase) enzyme activity were increased during fatigue.ConclusionsC60FAS leads to reduction in the recovery time of the muscle contraction force and to increase in the time of active muscle functioning before appearance of steady fatigue effects. Therefore, it is possible that C60FAS affects the prooxidant-antioxidant muscle tissue homeostasis, subsequently increasing muscle endurance.

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“…Homozygotic mice lacking mitochondrial PRX3 isoform are viable with no signs of muscle atrophy, although this mouse model showed an increase in skeletal muscle mitochondrial ROS, altered mitochondrial morphology and decreased muscle fatigue resistance. 272 These observations indicate that, although lack of PRX3 does not induce atrophy, it plays a crucial role in the contractile function of skeletal muscle by regulating the mitochondrial redox environment. 272 Additional recent studies undertaken in the field of metabolomics have shown that, although homozygotic mice lacking either mitochondrial TRX2 247 or TRX1 246 have embryonic lethal phenotypes, specific deletion of TRXinteracting protein in muscle specific knockout mice induces a reduction in exercise tolerance 279 by maintaining the redox balance during exercise and preserving mitochondrial capacity to switch substrates during glucose deprivation.…”

Section: Genetic Modification Of Mitochondrial Redox Systems To Studymentioning

confidence: 93%

Section: Non‐enzymatic Key Antioxidants That Contribute To the Maintementioning

confidence: 96%

Redox homeostasis and age‐related deficits in neuromuscular integrity and function

Sakellariou

Lightfoot

Earl

et al. 2017

J cachexia sarcopenia muscle

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Skeletal muscle is a major site of metabolic activity and is the most abundant tissue in the human body. Age‐related muscle atrophy (sarcopenia) and weakness, characterized by progressive loss of lean muscle mass and function, is a major contributor to morbidity and has a profound effect on the quality of life of older people. With a continuously growing older population (estimated 2 billion of people aged >60 by 2050), demand for medical and social care due to functional deficits, associated with neuromuscular ageing, will inevitably increase. Despite the importance of this ‘epidemic’ problem, the primary biochemical and molecular mechanisms underlying age‐related deficits in neuromuscular integrity and function have not been fully determined. Skeletal muscle generates reactive oxygen and nitrogen species (RONS) from a variety of subcellular sources, and age‐associated oxidative damage has been suggested to be a major factor contributing to the initiation and progression of muscle atrophy inherent with ageing. RONS can modulate a variety of intracellular signal transduction processes, and disruption of these events over time due to altered redox control has been proposed as an underlying mechanism of ageing. The role of oxidants in ageing has been extensively examined in different model organisms that have undergone genetic manipulations with inconsistent findings. Transgenic and knockout rodent studies have provided insight into the function of RONS regulatory systems in neuromuscular ageing. This review summarizes almost 30 years of research in the field of redox homeostasis and muscle ageing, providing a detailed discussion of the experimental approaches that have been undertaken in murine models to examine the role of redox regulation in age‐related muscle atrophy and weakness.

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Peroxiredoxin 3 has a crucial role in the contractile function of skeletal muscle by regulating mitochondrial homeostasis

Cited by 45 publications

References 39 publications

Mitochondrial peroxiredoxins are essential in regulating the relationship between Drosophila immunity and aging

Mitochondrial peroxiredoxins are essential in regulating the relationship between Drosophila immunity and aging

C60 fullerene as promising therapeutic agent for correcting and preventing skeletal muscle fatigue

Redox homeostasis and age‐related deficits in neuromuscular integrity and function

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