Cytoglobin modulates myogenic progenitor cell viability and muscle regeneration

Singh, Sarvjeet; Canseco, Diana C.; Manda, Shilpa M.; Shelton, John M.; Chirumamilla, Rajendra R.; Goetsch, Sean C.; Qiu, Ye; Gerard, Robert D.; Schneider, Jay W.; Richardson, James A.; Rothermel, Beverly A.; Mammen, Pradeep P.A.

doi:10.1073/pnas.1314962111

Cited by 61 publications

(67 citation statements)

References 85 publications

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“…Future studies using Cygb null mice (20,48) would be highly beneficially for studying the fate/function of neurons expressing PV, HO-1, SOMA and VIP. These studies will show whether a lack of Cygb affects neuronal survival or normal cell physiology by using these four proteins as markers.…”

Section: Discussionmentioning

confidence: 99%

“…The Cygb expression patterns in the mouse brain were recently determined to be identical in the rat and human brain, demonstrating that the rodent brain can be used as a translational model for studying Cygb in humans, at least at the anatomical level (12,13). The function of Cygb remains largely unknown, but several studies have linked Cygb to reactive oxygen/nitrogen species (RNS) nitric oxide (NO) scavenging (14)(15)(16)(17)(18)(19)(20). Furthermore, Cygb overexpression protects against ischemic cell death in vivo (21), although not when expressed at endogenous levels (22).…”

Section: Introductionmentioning

confidence: 99%

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Neurochemical phenotype of cytoglobin-expressing neurons in the rat hippocampus

2014

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Abstract. Cytoglobin (Cygb), a novel oxygen-binding protein, is expressed in the majority of tissues and has been proposed to function in nitric oxide (NO) metabolism in the vasculature and to have cytoprotective properties. However, the overall functions of Cygb remain elusive. Cygb is also expressed in a subpopulation of brain neurons. Recently, it has been shown that stress upregulates Cygb expression in the brain and the majority of neuronal nitric oxide synthase (nNOS)-positive neurons, an enzyme that produces NO, co-express Cygb. However, there are more neurons expressing Cygb than nNOS, thus a large number of Cygb neurons remain uncharacterized by the neurochemical content. The aim of the present study was to provide an additional and more detailed neurochemical phenotype of Cygb-expressing neurons in the rat hippocampus. The rat hippocampus was chosen due to the abundance of Cygb, as well as this limbic structure being an important target in a number of neurodegenerative diseases. Using triple immunohistochemistry, it was demonstrated that nearly all the parvalbumin-and heme oxygenase 1-positive neurons co-express Cygb and to a large extent, these neuron populations are distinct from the population of Cygb neurons co-expressing nNOS. Furthermore, it was shown that the majority of neurons expressing somastostatin and vasoactive intestinal peptide also co-express Cygb and nNOS. Detailed information regarding the neurochemical phenotype of Cygb neurons in the hippocampus can be a valuable tool in determining the function of Cygb in the brain.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Neurochemical phenotype of cytoglobin-expressing neurons in the rat hippocampus

2014

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“…Apoptosis in the skeletal muscle is low at rest, whereas skeletal muscle injury causes apoptosis and necrosis (307) and is associated with ROS production (341). Therefore, the protection of MuSCs from cytotoxic damage is crucial to ensure efficient regeneration.…”

Section: Redox Regulation Of Muscs During Skeletal Muscle Regenementioning

confidence: 99%

Redox Control of Skeletal Muscle Regeneration

Moal

Pialoux

Juban

et al. 2017

Antioxidants & Redox Signaling

148

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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“…Furthermore, transient Mb overexpression in myoblast led to enhance respiratory capacities of muscle mitochondria through specifically increase in complex IV activity (Yamada et al, 2016). Moreover, the increase in the expression of nuclear encoded mitochondrial genes correlates with Mb upregulation in both mRNA and protein (Garry et al, 1996;Kim et al, 1995), and Mb expression also links with the onset of differentiation (Kanatous & Mammen, 2010;Singh et al, 2014). These new evidence suggest that Mb is required for mitochondrial respiration during differentiation, and colocalization of Mb with/within the mitochondria contributes augmentation of mitochondrial respiration capacity via specifically regulated the activity of complex IV in skeletal muscles.…”

Section: Interaction Of Myoglobin With Mitochondria As Oxygen Mediatormentioning

confidence: 99%

Mitochondrial Biogenesis Induced by Exercise and Nutrients: Implication for Performance and Health Benefits

Masuda

Jue

Hamidie

2017

IJOST

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The skeletal muscle occupies about 40% of body mass, one of the largest organs in the body, and it has great plasticity in response to physiological stressors and then alters the contractile and metabolic properties of the muscles. Therefore, healthy status of muscle affects health status of whole body. Mitochondria are abundantly present in mammalian muscle cells, known as the power plants of the cell to generate adenosine triphosphate (ATP) with oxygen. The muscle health depends on the mitochondrial function. In aging and some of metabolic disease states, the mitochondrial function is defected. Some parts of this defect result from lower physical activity and nutritional status. The exercise is well-known as a major strategy to induce mitochondrial biogenesis and upregulation of the mitochondrial function. Recently some nutrients are also suggested as ligands for transcription of the mitochondrial proteins. We also recently found insight of protein interaction with mitochondria that will possibly augment mitochondrial respiratory potential. The present review article introduces some recent research evidences relating to mitochondrial quality control, mitochondrial biogenesis mediated by both exercise and nutrients and an interaction of protein with mitochondria to facilitate mitochondrial respiration.

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Cytoglobin modulates myogenic progenitor cell viability and muscle regeneration

Cited by 61 publications

References 85 publications

Neurochemical phenotype of cytoglobin-expressing neurons in the rat hippocampus

Neurochemical phenotype of cytoglobin-expressing neurons in the rat hippocampus

Redox Control of Skeletal Muscle Regeneration

Mitochondrial Biogenesis Induced by Exercise and Nutrients: Implication for Performance and Health Benefits

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