Nucleoprotein supplementation enhances the recovery of rat soleus mass with reloading after hindlimb unloading–induced atrophy via myonuclei accretion and increased protein synthesis

Nakanishi, Ryosuke; Hirayama, Yusuke; Tanaka, Minoru; Maeshige, Noriaki; Kondo, Hiroyo; Ishihara, Akihiko; Roy, Roland R.; Fujino, Hidemi

doi:10.1016/j.nutres.2016.10.007

Cited by 20 publications

(17 citation statements)

References 45 publications

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“…Denervation and cancer cachexia treatments activate the satellite cells [75,76]. Hindlimb suspension and fasting treatments impair satellite cell proliferation [77,78]. Immobilization decreases the number of satellite cells, whereas it increases the markers of satellite cell activation [79].…”

Section: Discussionmentioning

confidence: 99%

Expression Levels of Long Non-Coding RNAs Change in Models of Altered Muscle Activity and Muscle Mass

Hitachi

Nakatani

Funasaki

et al. 2020

IJMS

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Skeletal muscle is a highly plastic organ that is necessary for homeostasis and health of the human body. The size of skeletal muscle changes in response to intrinsic and extrinsic stimuli. Although protein-coding RNAs including myostatin, NF-κβ, and insulin-like growth factor-1 (IGF-1), have pivotal roles in determining the skeletal muscle mass, the role of long non-coding RNAs (lncRNAs) in the regulation of skeletal muscle mass remains to be elucidated. Here, we performed expression profiling of nine skeletal muscle differentiation-related lncRNAs (DRR, DUM1, linc-MD1, linc-YY1, LncMyod, Neat1, Myoparr, Malat1, and SRA) and three genomic imprinting-related lncRNAs (Gtl2, H19, and IG-DMR) in mouse skeletal muscle. The expression levels of these lncRNAs were examined by quantitative RT-PCR in six skeletal muscle atrophy models (denervation, casting, tail suspension, dexamethasone-administration, cancer cachexia, and fasting) and two skeletal muscle hypertrophy models (mechanical overload and deficiency of the myostatin gene). Cluster analyses of these lncRNA expression levels were successfully used to categorize the muscle atrophy models into two sub-groups. In addition, the expression of Gtl2, IG-DMR, and DUM1 was altered along with changes in the skeletal muscle size. The overview of the expression levels of lncRNAs in multiple muscle atrophy and hypertrophy models provides a novel insight into the role of lncRNAs in determining the skeletal muscle mass.

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Section: Discussionmentioning

confidence: 99%

Expression Levels of Long Non-Coding RNAs Change in Models of Altered Muscle Activity and Muscle Mass

Hitachi

Nakatani

Funasaki

et al. 2020

IJMS

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“…This evidence suggests that reduced satellite cell content and function may hinder the regenerative and regrowth responses that ordinarily follow periods of disuse. Similar decrements in oxidative (soleus) (2) and glycolytic (TA) (3) muscle satellite cell abundance during mechanical unloading offer evidence for coordinated regulation of satellite cell activity in metabolically-divergent skeletal muscles.…”

Section: Satellite Cell Interactions With Unloading/disuse and Denervmentioning

confidence: 95%

“…Nakanishi et al . exposed adult female rats to 14 days of bilateral HLS (2). Myosin heavy chain (MHC) type 1 and 2 fibers of the soleus muscle exhibited atrophy in concert with reduced satellite cell content.…”

Section: Satellite Cell Interactions With Unloading/disuse and Denervmentioning

confidence: 99%

“…Myosin heavy chain (MHC) type 1 and 2 fibers of the soleus muscle exhibited atrophy in concert with reduced satellite cell content. Pax7+ and MyoD+ satellite cell abundance was reduced in HLS animals, as was the frequency of myogenin+ differentiating satellite cells (2). These findings suggest muscle disuse impairs satellite cell proliferation and differentiation, and reduces general abundance.…”

Section: Satellite Cell Interactions With Unloading/disuse and Denervmentioning

confidence: 99%

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Altered satellite cell dynamics accompany skeletal muscle atrophy during chronic illness, disuse, and aging

McKenna

Fry

2017

Current Opinion in Clinical Nutrition &Amp; Metabolic Care

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Purpose of review This review explores recent research investigating the contribution of satellite cells (skeletal muscle stem cells) during muscle fiber atrophy as seen in periods of disuse, illness and aging. Recent findings Studies indicate reduced satellite cell activity and density in a variety of acute and chronic conditions characterized by robust muscle wasting. The direct contribution of satellite cells to unloading/denervation and chronic illness-induced atrophy remains controversial. Inflammation that accompanies acute trauma and illness likely impedes proper satellite cell differentiation and myogenesis, promoting the rapid onset of muscle wasting in these conditions. Transgenic mouse studies provide surprising evidence that age-related declines in satellite cell function and abundance are not causally related to the onset of sarcopenia in sedentary animals. Summary Recent clinical and pre-clinical studies indicate reduced abundance and dysregulated satellite cell activity that accompany muscle atrophy during periods of disuse, illness and aging, providing evidence for their therapeutic potential.

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“…During periods of unloading, preclinical models have shown a significant decline in the number of satellite cells. 62 Similarly, in humans, after periods of disuse, significant declines in satellite cell count have been observed, 3 in addition to moderate statistical relationships between augmentations in myofiber cross-sectional area and satellite cell content. 74 However, it should be noted that not all studies reach the same conclusion.…”

Section: Decoding the Mechanisms Of Disuse Muscle Atrophymentioning

confidence: 98%

Muscle Atrophy After ACL Injury: Implications for Clinical Practice

Lepley

Davi

Burland

et al. 2020

Sports Health: A Multidisciplinary Approach

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Context: Distinct from the muscle atrophy that develops from inactivity or disuse, atrophy that occurs after traumatic joint injury continues despite the patient being actively engaged in exercise. Recognizing the multitude of factors and cascade of events that are present and negatively influence the regulation of muscle mass after traumatic joint injury will likely enable clinicians to design more effective treatment strategies. To provide sports medicine practitioners with the best strategies to optimize muscle mass, the purpose of this clinical review is to discuss the predominant mechanisms that control muscle atrophy for disuse and posttraumatic scenarios, and to highlight how they differ. Evidence Acquisition: Articles that reported on disuse atrophy and muscle atrophy after traumatic joint injury were collected from peer-reviewed sources available on PubMed (2000 through December 2019). Search terms included the following: disuse muscle atrophy OR disuse muscle mass OR anterior cruciate ligament OR ACL AND mechanism OR muscle loss OR atrophy OR neurological disruption OR rehabilitation OR exercise. Study Design: Clinical review. Level of Evidence: Level 5. Results: We highlight that (1) muscle atrophy after traumatic joint injury is due to a broad range of atrophy-inducing factors that are resistant to standard resistance exercises and need to be effectively targeted with treatments and (2) neurological disruptions after traumatic joint injury uncouple the nervous system from muscle tissue, contributing to a more complex manifestation of muscle loss as well as degraded tissue quality. Conclusion: Atrophy occurring after traumatic joint injury is distinctly different from the muscle atrophy that develops from disuse and is likely due to the broad range of atrophy-inducing factors that are present after injury. Clinicians must challenge the standard prescriptive approach to combating muscle atrophy from simply prescribing physical activity to targeting the neurophysiological origins of muscle atrophy after traumatic joint injury.

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Nucleoprotein supplementation enhances the recovery of rat soleus mass with reloading after hindlimb unloading–induced atrophy via myonuclei accretion and increased protein synthesis

Cited by 20 publications

References 45 publications

Expression Levels of Long Non-Coding RNAs Change in Models of Altered Muscle Activity and Muscle Mass

Expression Levels of Long Non-Coding RNAs Change in Models of Altered Muscle Activity and Muscle Mass

Altered satellite cell dynamics accompany skeletal muscle atrophy during chronic illness, disuse, and aging

Muscle Atrophy After ACL Injury: Implications for Clinical Practice

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