Skeletal muscle adaptations to microgravity exposure in the mouse

Harrison, Brooke C.; Allen, David L.; Girten, B.; Stodieck, Louis S.; Kostenuik, Paul J.; Bateman, Ted A.; Morony, Sean; Leinwand, Leslie A.

doi:10.1152/japplphysiol.00603.2003

Cited by 78 publications

(85 citation statements)

References 45 publications

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“…Moreover, we have found that denervation combined with tenotomy, which, in addition, suppresses passive muscle tension, had no further effects on the percentage of MHC-1 ϩ muscle fibers, despite a greater muscle fiber atrophy and a reduction in oxidative capacity. Other models of reduced neuromuscular activity (such as hindlimb suspension and microgravity) induced no change in the slow phenotype in the soleus muscles of C57BL/6 and CD1 mice (24,51,59). Therefore, it is tempting to conclude that neuromuscular activity, including neural input, passive stretch, and mechanical load, are not necessary for the maintenance of a normal expression of MHC-1 protein in mouse soleus muscles (the present study, Refs.…”

Section: Discussionmentioning

confidence: 58%

Slow myosin heavy chain expression in the absence of muscle activity

Agbulut

Vignaud²,

Hourdé³

et al. 2009

American Journal of Physiology-Cell Physiology

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Innervation has been generally accepted to be a major factor involved in both triggering and maintaining the expression of slow myosin heavy chain (MHC-1) in skeletal muscle. However, previous findings from our laboratory have suggested that, in the mouse, this is not always the case (30). Based on these results, we hypothesized that neurotomy would not markedly reduced the expression of MHC-1 protein in the mouse soleus muscles. In addition, other cellular, biochemical, and functional parameters were also studied in these denervated soleus muscles to complete our study. Our results show that denervation reduced neither the relative amount of MHC-1 protein, nor the percentage of muscle fibers expressing MHC-1 protein (P Ͼ 0.05). The fact that MHC-1 protein did not respond to muscle inactivity was confirmed in three different mouse strains (129/SV, C57BL/6, and CD1). In contrast, all of the other histological, biochemical, and functional muscle parameters were markedly altered by denervation. Cross-sectional area (CSA) of muscle fibers, maximal tetanic isometric force, maximal velocity of shortening, maximal power, and citrate synthase activity were all reduced in denervated muscles compared with innervated muscles (P Ͻ 0.05). Contraction and one-half relaxation times of the twitch were also increased by denervation (P Ͻ 0.05). Addition of tenotomy to denervation had no further effect on the relative expression of MHC-1 protein (P Ͼ 0.05), despite a greater reduction in CSA and citrate synthase activity (P Ͻ 0.05). In conclusion, a deficit in neural input leads to marked atrophy and reduction in performance in mouse soleus muscles. However, the maintenance of the relative expression of slow MHC protein is independent of neuromuscular activity in mice. skeletal muscle; tenotomy; force; slow myosin heavy chain; power; velocity of shortening; oxidative capacity; atrophy NEUROMUSCULAR ACTIVITY, INCLUDING both the neural and mechanical aspects, plays an important role in skeletal muscle physiology. It is now well established that increased chronic neuromuscular activity (physical training and electrical stimulation) induces beneficial adaptations in both muscle structure and function (for review, Refs. 23, 46). Moreover, there is a very large body of information showing that reduced neuromuscular activity (i.e., denervation, spinal cord isolation, disuse) causes important impairments in muscle function (for review, Refs. 20,41). For example, a reduction or the elimination of neural input results in muscle atrophy. Denervated slow muscles produce less maximal force and power, and the kinetics of the twitch is slower. This is accompanied by a reduction in oxidative capacity and a decrease in the relative expression of slow myosin heavy chain (MHC-1) protein (for review, Refs. 41, 53). However, it should be noted that most of this experimental data is derived from experiments on rats.MHC-1 protein is one of the major contractile proteins and is important for muscle function. A high level of MHC-1 expression in skeletal m...

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Section: Discussionmentioning

confidence: 58%

Slow myosin heavy chain expression in the absence of muscle activity

Agbulut

Vignaud²,

Hourdé³

et al. 2009

American Journal of Physiology-Cell Physiology

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“…Weightlessness also reduces functional capacity in limb skeletal muscle of animals including humans (Ilyina-Kakueva et al, 1976;Widrick et al, 1999;Fitts et al, 2000). In vertebrate skeletal muscle, the greatest changes are observed in the limb antigravity muscles, such as soleus (Riley et al, 1987;Widrick et al, 1999;Harrison et al, 2003). Major changes in these muscles alter the expression of muscle protein isoforms, mainly myosin heavy chains (MHCs).…”

Section: Introductionmentioning

confidence: 99%

“…Major changes in these muscles alter the expression of muscle protein isoforms, mainly myosin heavy chains (MHCs). After microgravity exposure, the fibers that express slow type MHCs are decreased and those that express fast type MHCs are increased in soleus slow muscle (Caiozzo et al, 1996;Harrison et al, 2003). At the molecular level, distinct β-MHC promoter sequences mediate β-MHC expression in response to overload and unloading in mice (McCarthy et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

Spaceflight results in increase of thick filament but not thin filament proteins in the paramyosin mutant of Caenorhabditis elegans

Adachi

Takaya

Kuriyama

et al. 2008

Advances in Space Research

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We have investigated the effect of microgravity during spaceflight on body-wall muscle fiber size and muscle proteins in the paramyosin mutant of Caenorhabditis elegans.Both mutant and wild-type strains were subjected to 10 days of microgravity during spaceflight and compared to ground control groups. No significant change in muscle fiber size or quantity of the protein was observed in wild-type worms; where as atrophy of body-wall muscle and an increase in thick filament proteins were observed in the paramyosin mutant unc-15(e73) animals after spaceflight. We conclude that the mutant with abnormal muscle responded to microgravity by increasing the total amount of muscle protein in order to compensate for the loss of muscle function.

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“…When exposed to the microgravity of spaceflight, muscles developed on Earth have been shown to display changes in morphology, contractile function and myosin heavy chain (MHC) gene expression (Caiozzo et al, 1994;Caiozzo et al, 1996;Criswell et al, 1996;Day et al, 1995;Edgerton et al, 1995;Fitts et al, 2000;Harrison et al, 2003). Recently, it was shown that cultured embryonic avian muscle cells are directly responsive to spaceflight, undergoing atrophy as the result of decreased protein synthesis (Vandenburgh et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

Decreased expression of myogenic transcription factors and myosin heavy chains inCaenorhabditis elegansmuscles developed during spaceflight

Higashibata

Szewczyk

Conley

et al. 2006

Journal of Experimental Biology

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SUMMARY The molecular mechanisms underlying muscle atrophy during spaceflight are not well understood. We have analyzed the effects of a 10-day spaceflight on Caenorhabditis elegans muscle development. DNA microarray, real-time quantitative PCR, and quantitative western blot analyses revealed that the amount of MHC in both body-wall and pharyngeal muscle decrease in response to spaceflight. Decreased transcription of the body-wall myogenic transcription factor HLH-1 (CeMyoD) and of the three pharyngeal myogenic transcription factors, PEB-1, CEH-22 and PHA-4 were also observed. Upon return to Earth animals displayed reduced rates of movement, indicating a functional defect. These results demonstrate that C. elegans muscle development is altered in response to spaceflight. This altered development occurs at the level of gene transcription and was observed in the presence of innervation,not simply in isolated cells. This important finding coupled with past observations of decreased levels of the same myogenic transcription factions in vertebrates after spaceflight raises the possibility that altered muscle development is a contributing factor to spaceflight-induced muscle atrophy in vertebrates.

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Skeletal muscle adaptations to microgravity exposure in the mouse

Cited by 78 publications

References 45 publications

Slow myosin heavy chain expression in the absence of muscle activity

Slow myosin heavy chain expression in the absence of muscle activity

Spaceflight results in increase of thick filament but not thin filament proteins in the paramyosin mutant of Caenorhabditis elegans

Decreased expression of myogenic transcription factors and myosin heavy chains inCaenorhabditis elegansmuscles developed during spaceflight

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