Regulation of Protein Synthesis and Skeletal Muscle Growth

The ribosome is the enzymatic macromolecular machine responsible for protein synthesis. The rates of protein synthesis are primarily dependent on translational efficiency and capacity. Ribosome biogenesis has emerged as an important regulator of skeletal muscle growth and maintenance by altering the translational capacity of the cell. Here, we provide evidence to support a central role for ribosome biogenesis in skeletal muscle growth during postnatal development and in response to resistance exercise training. Furthermore, we discuss the cellular signaling pathways regulating ribosome biogenesis, discuss how myonuclear accretion affects translational capacity, and explore future areas of investigation within the field.

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mTORC1 Mediates Lysine-Induced Satellite Cell Activation to Promote Skeletal Muscle Growth

Cells ◽

10.3390/cells8121549 ◽

2019 ◽

Vol 8 (12) ◽

pp. 1549 ◽

Cited By ~ 3

Author(s):

Cheng-long Jin ◽

Jin-ling Ye ◽

Jinzeng Yang ◽

Chun-qi Gao ◽

Hui-chao Yan ◽

...

Keyword(s):

Skeletal Muscle ◽

Protein Synthesis ◽

Cell Activation ◽

Muscle Growth ◽

Mammalian Target Of Rapamycin ◽

Absolute Quantitation ◽

Skeletal Muscle Growth ◽

Mtorc1 Pathway

As the first limiting amino acid, lysine (Lys) has been thought to promote muscle fiber hypertrophy by increasing protein synthesis. However, the functions of Lys seem far more complex than that. Despite the fact that satellite cells (SCs) play an important role in skeletal muscle growth, the communication between Lys and SCs remains unclear. In this study, we investigated whether SCs participate directly in Lys-induced skeletal muscle growth and whether the mammalian target of rapamycin complex 1 (mTORC1) pathway was activated both in vivo and in vitro to mediate SC functions in response to Lys supplementation. Subsequently, the skeletal muscle growth of piglets was controlled by dietary Lys supplementation. Isobaric tag for relative and absolute quantitation (iTRAQ) analysis showed activated SCs were required for longissimus dorsi muscle growth, and this effect was accompanied by mTORC1 pathway upregulation. Furthermore, SC proliferation was governed by medium Lys concentrations, and the mTORC1 pathway was significantly enhanced in vitro. After verifying that rapamycin inhibits the mTORC1 pathway and suppresses SC proliferation, we conclude that Lys is not only a molecular building block for protein synthesis but also a signal that activates SCs to manipulate muscle growth via the mTORC1 pathway.

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PSIX-29 JAK2-STAT3 Pathway Mediated Satellite Cell Apoptosis to Govern Skeletal Muscle Growth with Lysine

Journal of Animal Science ◽

10.1093/jas/skaa278.594 ◽

2020 ◽

Vol 98 (Supplement_4) ◽

pp. 334-334

Author(s):

Zhi-wen Song ◽

Cheng-long Jin ◽

Mao Ye ◽

Chun-qi Gao ◽

Hui-chao Yan ◽

...

Keyword(s):

Skeletal Muscle ◽

Muscle Growth ◽

Longissimus Dorsi ◽

Control Group ◽

Stat3 Pathway ◽

Skeletal Muscle Growth ◽

Longissimus Dorsi Muscle ◽

Dorsi Muscle ◽

Pathway Inhibition ◽

Induced Apoptosis

Abstract Apoptosis is programmed cell death that can be stimulated by external stress or nutrition restrictions. Lysine (Lys) is an essential amino acid for pig growth, and the relationship between Lys deficiency caused apoptosis and inhibition of skeletal muscle growth remains unknown. The objective of this study was to investigate whether apoptosis could be regulated by Lys supplementation and the potential mechanism. In current work, 30 male Duroc × Landrace × Large weaned piglets were divided randomly into 3 groups: control group (Lys 1.30%), Lys deficiency group (Lys 0.86%), and Lys rescue group (Lys 0.86%, 0-14d; 1.30%,15–28 d). The experiment lasted for 28 days, and on the morning of 29 d, piglets were slaughtered to collect samples. Isobaric tag for relative and absolute quantification (iTRAQ) proteomics analysis of the longissimus dorsi muscle showed that Janus family tyrosine kinase (JAK)-signal transducer and activator of transcription (STAT) pathway was involved in Lys deficiency-induced apoptosis and inhibited skeletal muscle growth. Meanwhile, western blotting results of the longissimus dorsi muscle demonstrated that Lys deficiency caused apoptosis (P < 0.05) with the JAK2-STAT3 pathway inhibition (P < 0.05). Interestingly, apoptosis was suppressed (P < 0.05), and the JAK2-STAT3 pathway was reactivated (P < 0.05) after Lys re-supplementation in longissimus dorsi muscle. In addition, results of satellite cells (SCs) isolated from the longissimus dorsi muscle of 5-day-old Landrace piglets showed that Lys deficiency-induced apoptosis (P < 0.05) was mediated by the JAK2-STAT3 pathway inhibition (P < 0.05). Moreover, the JAK2-STAT3 pathway was reactivated (P < 0.05) by Lys re-supplementation and suppressed apoptosis in SCs (P < 0.05), and this effect was blocked (P < 0.05) after SCs treated with AG-490 (a specific inhibitor of JAK2). Collectively, Lys inhibited apoptosis in SCs to govern skeletal muscle growth via the JAK2-STAT3 pathway.

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Fish growth in response to different feeding regimes and the related molecular mechanism on the changes in skeletal muscle growth in grass carp (Ctenopharyngodon idellus)

Aquaculture ◽

10.1016/j.aquaculture.2019.734295 ◽

2019 ◽

Vol 512 ◽

pp. 734295 ◽

Cited By ~ 3

Author(s):

Yingyan Xu ◽

Qingsong Tan ◽

Fanshuang Kong ◽

Haojie Yu ◽

Yanhong Zhu ◽

...

Keyword(s):

Skeletal Muscle ◽

Molecular Mechanism ◽

Grass Carp ◽

Muscle Growth ◽

Fish Growth ◽

Ctenopharyngodon Idellus ◽

Skeletal Muscle Growth ◽

Feeding Regimes

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Why exercise builds muscles: Titin mechanosensing controls skeletal muscle growth under load

Biophysical Journal ◽

10.1016/j.bpj.2021.07.023 ◽

2021 ◽

Author(s):

Neil Ibata ◽

Eugene M. Terentjev

Keyword(s):

Skeletal Muscle ◽

Muscle Growth ◽

Skeletal Muscle Growth

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Skeletal Muscle Growth, Enzyme Activities, and the Development of Thermogenesis: A Comparison between Altricial and Precocial Birds

Physiological Zoology ◽

10.1086/physzool.66.4.30163803 ◽

1993 ◽

Vol 66 (4) ◽

pp. 455-473 ◽

Cited By ~ 71

Author(s):

In-Ho Choi ◽

Robert E. Ricklefs ◽

Russell E. Shea

Keyword(s):

Skeletal Muscle ◽

Enzyme Activities ◽

Muscle Growth ◽

Skeletal Muscle Growth ◽

Precocial Birds

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Anemic Hypoxemia Reduces Myoblast Proliferation and Muscle Growth in Late Gestation Fetal Sheep

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00342.2020 ◽

2021 ◽

Author(s):

Paul J. Rozance ◽

Stephanie R Wesolowski ◽

Sonnet S. Jonker ◽

Laura D Brown

Keyword(s):

Skeletal Muscle ◽

Mrna Expression ◽

Muscle Growth ◽

Late Gestation ◽

Whole Body ◽

Myoblast Differentiation ◽

Fetal Sheep ◽

Body Protein ◽

Skeletal Muscle Growth ◽

Myoblast Proliferation

Fetal skeletal muscle growth requires myoblast proliferation, differentiation, and fusion into myofibers in addition to protein accretion for fiber hypertrophy. Oxygen is an important regulator of this process. Therefore, we hypothesized that fetal anemic hypoxemia would inhibit skeletal muscle growth. Studies were performed in late gestation fetal sheep that were bled to anemic, and therefore hypoxemic, conditions beginning at ~125 days of gestation (term = 148 days) for 9 ± 0 days (n=19) and compared to control fetuses (n=16). A metabolic study was performed on gestational day ~134 to measure fetal protein kinetic rates. Myoblast proliferation and myofiber area were determined in biceps femoris (BF), tibialis anterior (TA), and flexor digitorum superficialis (FDS) muscles. mRNA expression of muscle regulatory factors was determined in BF. Fetal arterial hematocrit and oxygen content were 28% and 52% lower, respectively, in anemic fetuses. Fetal weight and whole-body protein synthesis, breakdown, and accretion rates were not different between groups. Hindlimb length, however, was 7% shorter in anemic fetuses. TA and FDS muscles weighed less and FDS myofiber area was smaller in anemic fetuses compared to controls. The percentage of Pax7+ myoblasts that expressed Ki67 was lower in BF and tended to be lower in FDS from anemic fetuses indicating reduced myoblast proliferation. There was less MYOD and MYF6 mRNA expression in anemic vs. control BF consistent with reduced myoblast differentiation. These results indicate that fetal anemic hypoxemia reduced muscle growth. We speculate that fetal muscle growth may be improved by strategies that increase oxygen availability.

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