Nitric-oxide Synthase Is a Mechanical Signal Transducer That Modulates Talin and Vinculin Expression

Tidball, James G.; Spencer, Melissa J.; Wehling, M.; Lavergne, Éliane

doi:10.1074/jbc.274.46.33155

Cited by 53 publications

(38 citation statements)

References 43 publications

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“…Inducible NOS isoenzyme is involved in the immune response and is primarily expressed in skeletal muscle in response to inflammatory conditions or a septic challenge 114, 115. NO has shown to regulate cytoskeletal proteins,116 and nNOS isoform, strongly expressed in glycolytic muscle fibres,117 has been reported as the prime source of NO release from skeletal muscle 118. The importance of NO signalling in muscle physiology is highlighted in mdx mice119 and humans with Duchenne muscular dystrophy 112, 120.…”

Section: Chemistry Of Reactive Oxygen and Nitrogen Species Produced Bmentioning

confidence: 99%

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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Section: Chemistry Of Reactive Oxygen and Nitrogen Species Produced Bmentioning

confidence: 99%

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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“…Neuronal NOS is activated by both mechanical force and pressure. The subsequent production of NO induces the expression of the two cytoskeletal proteins, talin and vinculin, resulting in muscle hypertrophy (Tidball et al, 1999). NO produced by nNOS also activates muscle satellite cells, although the molecular components of this pathway are unknown (Anderson, 2000).…”

Section: Nitric Oxide and Muscle Hypertrophymentioning

confidence: 99%

When bad things happen to good fish: the loss of hemoglobin and myoglobin expression in Antarctic icefishes

Sidell

O’Brien

2006

Journal of Experimental Biology

252

227

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SUMMARY The Antarctic icefishes (Family Channichthyidae) provide excellent examples of unique traits that can arise in a chronically cold and isolated environment. Their loss of hemoglobin (Hb) expression, and in some cases, loss of myoglobin (Mb) expression, has taught us much about the function of these proteins. Although absences of the proteins are fixed traits in icefishes, the losses do not appear to be of adaptive value. Contrary to some suggestions,loss of Hb has led to higher energetic costs for circulating blood, and losses of Mb have reduced cardiac performance. Moreover, losses of Hb and Mb have resulted in extensive modifications to the cardiovascular system to ensure adequate oxygen delivery to working muscles. Recent studies suggest that losses of Hb and Mb, and their associated nitric oxide (NO)-oxygenase activities, may have accelerated the development and evolution of these cardiovascular modifications. The high levels of NO that should occur in the absence of Hb and Mb have been shown in other animal groups to lead to an increase in tissue vascularization, an increase in the lumenal diameter of blood vessels, and an increase in mitochondrial densities. These characteristics are all hallmark traits of Antarctic icefishes. Homeostatic feedback mechanisms thus may have accelerated evolution of the pronounced cardiovascular traits of Antarctic icefishes.

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“…For example, mechanical force affects the expression of several cytoskeletal genes including the ␣-skeletal and ␣-smooth muscle actin isoforms (1) as well as the actin-binding proteins talin and vinculin (2). Mechanical force induction of cytoskeletal protein expression has been examined most prominently reported for smooth muscle cells (3,4), but the transcriptional regulation of actin-binding proteins in nonmuscle cells has not been evaluated in detail.…”

mentioning

confidence: 99%

Cytoprotection against Mechanical Forces Delivered through β1 Integrins Requires Induction of Filamin A

D’Addario

Arora

Fan

et al. 2001

Journal of Biological Chemistry

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Cells in mechanically active environments can activate cytoprotective mechanisms to maintain membrane integrity in the face of potentially lethal applied forces. Cytoprotection may be mediated by expression of membrane-associated cytoskeletal proteins including filamin A, an actin-binding protein that increases the rigidity of the subcortical actin cytoskeleton. In this study, we tested the hypotheses that applied forces induce the expression of filamin A specifically and that this putative protective response inhibits cell death. Magnetically generated forces were applied to proteincoated magnetite beads bound to human gingival fibroblasts, cells with constitutively low basal levels of filamin A mRNA and protein. Forces applied through collagen or fibronectin, but not bovine serum albumin or poly-L-lysine-coated beads, increased mRNA and protein content of filamin A by 3-7-fold. Forces had no effect on the expression of other filamin isotypes or other cytoskeletal proteins. This effect was dependent on the duration of force and was blocked by anti-␤ 1 integrin antibodies. Force also stimulated a 60% increase in expression of luciferase under the control of a filamin A promoter in transiently transfected Rat2 fibroblasts and was dependent on Sp1 transcription factor binding sites located immediately upstream of the transcription start site. Experiments with actinomycin D-treated cells showed that the increased filamin A expression after force application was due in part to prolongation of mRNA half-life. Antisense filamin oligonucleotides blocked force-induced filamin A expression and increased cell death by >2-fold above controls. The forceinduced regulation of filamin A was dependent on intact actin filaments. We conclude that cells from mechanically active environments can couple diverse signals from forces applied through ␤-integrins to up-regulate the production of cytoprotective cytoskeletal proteins, typified by filamin A.

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Nitric-oxide Synthase Is a Mechanical Signal Transducer That Modulates Talin and Vinculin Expression

Cited by 53 publications

References 43 publications

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

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

When bad things happen to good fish: the loss of hemoglobin and myoglobin expression in Antarctic icefishes

Cytoprotection against Mechanical Forces Delivered through β1 Integrins Requires Induction of Filamin A

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