A simplified immunohistochemical classification of skeletal muscle fibres in mouse

Kammoun, Malek; Cassar-Malek, Isabelle; Meunier, Bruno; Picard, Brigitte

doi:10.4081/ejh.2014.2254

Cited by 91 publications

(89 citation statements)

References 27 publications

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“…Second, the gene expression was analyzed based on a single skeletal muscle, the TA muscle. TA is composed of predominantly type II fibers, which is also the predominant muscle fiber type in the hind limb muscles of mice . Soleus (SOL) was not used for the analysis due to the fact that mouse SOL contains a mixture of type I and type II muscle fibers, which is in contrast to other mammals (mainly type I muscle fibers) .…”

Section: Discussionmentioning

confidence: 99%

Altered bone‐regulating myokine expression in skeletal muscle Of Duchenne muscular dystrophy mouse models

et al. 2018

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Section: Discussionmentioning

confidence: 99%

Altered bone‐regulating myokine expression in skeletal muscle Of Duchenne muscular dystrophy mouse models

et al. 2018

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“…For example, the data described above were derived from measurements in the gastrocnemius of rats and tibialis anterior of mice, which are composed of both slow-and fast-twitch fibers (55,63). Whether REDD1 possesses a fiber type-specific effect with refeeding remains to be determined.…”

Section: Role Of Redd1 During Physiological Conditionsmentioning

confidence: 99%

Emerging role for regulated in development and DNA damage 1 (REDD1) in the regulation of skeletal muscle metabolism

Gordon

Steiner

Williamson

et al. 2016

American Journal of Physiology-Endocrinology and Metabolism

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SR.Emerging role for regulated in development and DNA damage 1 (REDD1) in the regulation of skeletal muscle metabolism. Am J Physiol Endocrinol Metab 311: E157-E174, 2016. First published May 17, 2016; doi:10.1152/ajpendo.00059.2016.-Since its discovery, the protein regulated in development and DNA damage 1 (REDD1) has been implicated in the cellular response to various stressors. Most notably, its role as a repressor of signaling through the central metabolic regulator, the mechanistic target of rapamycin in complex 1 (mTORC1) has gained considerable attention. Not surprisingly, changes in REDD1 mRNA and protein have been observed in skeletal muscle under various physiological conditions (e.g., nutrient consumption and resistance exercise) and pathological conditions (e.g., sepsis, alcoholism, diabetes, obesity) suggesting a role for REDD1 in regulating mTORC1-dependent skeletal muscle protein metabolism. Our understanding of the causative role of REDD1 in skeletal muscle metabolism is increasing mostly due to the availability of genetically modified mice in which the REDD1 gene is disrupted. Results from such studies provide support for an important role for REDD1 in the regulation of mTORC1 as well as reveal unexplored functions of this protein in relation to other aspects of skeletal muscle metabolism. The goal of this work is to provide a comprehensive review of the role of REDD1 (and its paralog REDD2) in skeletal muscle during both physiological and pathological conditions. muscle mass; RTP801; DDIT4; dig2 MAINTAINING SKELETAL MUSCLE MASS is of critical importance to many groups of people, ranging from athletes trying to accrete muscle protein to individuals trying to minimize protein loss with catabolic diseases such as cancer, sarcopenia, HIV/AIDS, sepsis, alcoholism, and diabetes. It is widely accepted that an increase in muscle mass and strength enhances physical performance in young, healthy individuals (16,47,97), and maintenance of skeletal muscle mass and strength in catabolic states is associated with decreased mortality (56,80,91,94,107). Moreover, in many catabolic conditions, current nutritional and pharmacological interventions are unable to prevent or reverse the erosion of muscle mass, thus presenting a barrier to improved patient care (122, 123). Therefore, a more complete understanding of how skeletal muscle mass is regulated is central to minimize its loss and/or speed recovery following disease in which muscle mass is compromised.The protein regulated in development and DNA damage 1 (REDD1) has been identified as a key regulator of skeletal muscle mass. For example, skeletal muscle-specific overexpression of REDD1 via electroporation reduces muscle fiber cross-sectional area (CSA) (35), and using mice with a global disruption of the REDD1 gene [hereafter referred to as REDD1 knockout (KO) mice] has implicated REDD1 as an important protein in muscle metabolism under both physiological and pathological conditions. As a thorough phenotypic description of the skeletal muscle from mice with ...

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“…This variation may be caused by various compositions of muscle fiber type in specific muscles. For instance, TA and EDL contain more fast‐glycolytic type IIb fiber than SOL, which mainly contains slow‐oxidative type I and fast‐oxidative type IIa (42). In addition, it has been revealed that food deprivation could preferentially affect protein turnover in fast‐glycolytic fibers (43, 44).…”

Section: Discussionmentioning

confidence: 99%

TRB3 regulates skeletal muscle mass in food deprivation–induced atrophy

et al. 2019

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Tribbles 3 (TRB3) is a pseudokinase that has been found in multiple tissues in response to various stress stimuli, such as nutrient deprivation and endoplasmic reticulum (ER) stress. We recently found that TRB3 has the potential to regulate skeletal muscle mass at the basal state. However, it has not yet been explored whether TRB3 regulates skeletal muscle mass under atrophic conditions. Here, we report that food deprivation for 48 h in mice significantly reduces muscle mass by ∼15% and increases TRB3 expression, which is associated with increased ER stress. Interestingly, inhibition of ER stress in C2C12 myotubes reduces food deprivation–induced expression of TRB3 and muscle‐specific E3‐ubiquitin ligases. In further in vivo experiments, muscle‐specific TRB3 transgenic mice increase food deprivation–induced muscle atrophy compared with wild‐type (WT) littermates presumably by the increased proteolysis. On the other hand, TRB3 knockout mice ameliorate food deprivation–induced atrophy compared with WT littermates by preserving a higher protein synthesis rate. These results indicate that TRB3 plays a pivotal role in skeletal muscle mass regulation under food deprivation–induced muscle atrophy and TRB3 could be a pharmaceutical target to prevent skeletal muscle atrophy.—Choi, R. H., McConahay, A., Silvestre, J. G., Moriscot, A. S., Carson, J. A., Koh, H.‐J. TRB3 regulates skeletal muscle mass in food deprivation–induced atrophy. FASEB J. 33, 5654–5666 (2019). http://www.fasebj.org

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A simplified immunohistochemical classification of skeletal muscle fibres in mouse

Cited by 91 publications

References 27 publications

Altered bone‐regulating myokine expression in skeletal muscle Of Duchenne muscular dystrophy mouse models

Altered bone‐regulating myokine expression in skeletal muscle Of Duchenne muscular dystrophy mouse models

Emerging role for regulated in development and DNA damage 1 (REDD1) in the regulation of skeletal muscle metabolism

TRB3 regulates skeletal muscle mass in food deprivation–induced atrophy

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