scholarly journals THE VICIOUS CYCLE OF MYOSTATIN SIGNALING IN SARCOPENIC OBESITY: MYOSTATIN ROLE IN SKELETAL MUSCLE GROWTH, INSULIN SIGNALING AND IMPLICATIONS FOR CLINICAL TRIALS

2017 ◽  
pp. 1-7
Author(s):  
L.A. CONSITT ◽  
B.C. CLARK
Keyword(s):  
Skeletal Muscle ◽  
Clinical Trials ◽  
Insulin Signaling ◽  
Muscle Growth ◽  
Sarcopenic Obesity ◽  
Health Concern ◽  
Potential Candidate ◽  
Skeletal Muscle Growth ◽  
Age Related

The age-related loss of skeletal muscle (sarcopenia) is a major health concern as it is associated with physical disability, metabolic impairments, and increased mortality. The coexistence of sarcopenia with obesity, termed ‘sarcopenic obesity’, contributes to skeletal muscle insulin resistance and the development of type 2 diabetes, a disease prevalent with advancing age. Despite this knowledge, the mechanisms contributing to sarcopenic obesity remain poorly understood, preventing the development of targeted therapeutics. This article will discuss the clinical and physiological consequences of sarcopenic obesity and propose myostatin as a potential candidate contributing to this condition. A special emphasis will be placed on examining the role of myostatin signaling in impairing both skeletal muscle growth and insulin signaling. In addition, the role of myostatin in regulating muscle-to fat cross talk, further exacerbating metabolic dysfunction in the elderly, will be highlighted. Lastly, we discuss how this knowledge has implications for the design of myostatin-inhibitor clinical trials.

scholarly journals The Possible Role of Complete Loss of Myostatin in Limiting Excessive Proliferation of Muscle Cells (C2C12) via Activation of MicroRNAs

2019 ◽  
Vol 20 (3) ◽  
pp. 643 ◽  
Author(s):  
Peixuan Huang ◽  
Daxin Pang ◽  
Kankan Wang ◽  
Aishi Xu ◽  
Chaogang Yao ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cell Proliferation ◽  
Muscle Growth ◽  
Interaction Network ◽  
Muscle Cells ◽  
Complete Loss ◽  
Skeletal Muscle Growth ◽  
Excessive Proliferation ◽  
Mouse Myoblast

Myostatin (MSTN) is a member of the TGF-β superfamily that negatively regulates skeletal muscle growth and differentiation. However, the mechanism by which complete MSTN deletion limits excessive proliferation of muscle cells remains unclear. In this study, we knocked out MSTN in mouse myoblast lines using a Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR/Cas9) system and sequenced the mRNA and miRNA transcriptomes. The results show that complete loss of MSTN upregulates seven miRNAs targeting an interaction network composed of 28 downregulated genes, including TGFB1, FOS and RB1. These genes are closely associated with tumorigenesis and cell proliferation. Our study suggests that complete loss of MSTN may limit excessive cell proliferation via activation of miRNAs. These data will contribute to the treatment of rhabdomyosarcoma (RMS).

scholarly journals 343 Wnt/β-catenin pathway is required for porcine satellite cell proliferation and differentiation to promote skeletal muscle growth

2019 ◽  
Vol 97 (Supplement_3) ◽  
pp. 97-97
Author(s):  
Zong-ming Zhang ◽  
Chun-qi Gao ◽  
Hui-chao Yan ◽  
Xiu-qi Wang
Keyword(s):  
Skeletal Muscle ◽  
Cell Proliferation ◽  
Satellite Cell ◽  
Muscle Growth ◽  
Control Group ◽  
Skeletal Muscle Growth ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation ◽  
Deficiency Group

Abstract Wnt/β-catenin plays a crucial role in skeletal muscle growth, but its specific mechanism still unclear. In this study, due to the distinct role of lysine in pig industry, we provided it as an entry point to investigate the role of Wnt/β-catenin in governing skeletal muscle growth. Firstly, total 18 weaned piglets were divided into three groups: control group, lysine deficiency group and lysine re-supplementation group (lysine levels added from 0.83% to 1.31% at 14 d). After 28 d experiment, all pigs were slaughtered to measure the change of Wnt/β-catenin in skeletal muscle. Secondly, satellite cell (SC) was isolated and cultured with Wnt activator, such as Wnt3a and WRN (Wnt3a, R-spondin1, Noggin) after lysine deficiency for 48 h to investigate cell proliferation and differentiation ability and the level of Wnt/β-catenin in different conditions. The results showed that compared with the control group, lysine deficiency significantly reduced longissimus dorsi muscle weight and Pax7 positive SC, and inhibited Wnt/β-catenin (P < 0.05). Fortunately, these restrictions were rescued to the control levels by lysine re-supplementation (P > 0.05). Meanwhile, compared with the lysine deficiency group, the MTT and western blotting assay showed cell proliferation ability was significantly increased with re-activated Wnt/β-catenin by re-supplemented lysine, Wnt3a or WRN (P < 0.05), respectively. Moreover, under the condition of cell differentiation, compared with the control group, cell fusion index was significantly decreased in the lysine deficiency group (P < 0.05), whereas it was significantly increased with lysine re-supplementation group, Wnt3a or WRN respective supplementation group in comparison with the lysine deficiency group (P < 0.05). In addition, compared with the lysine deficiency group, the protein levels of myogenic regulatory factors and Wnt/β-catenin pathway were also re-activated by re-supplemented lysine, Wnt3a or WRN (P < 0.05). Collectively, we found Wnt/β-catenin activation is required for porcine SC proliferation and differentiation to promote skeletal muscle growth.

Myonuclear accretion is a major determinant of avian skeletal muscle growth

1997 ◽  
Vol 272 (2) ◽  
pp. C565-C571 ◽  
Author(s):  
P. E. Mozdziak ◽  
E. Schultz ◽  
R. G. Cassens
Keyword(s):  
Skeletal Muscle ◽  
Mitotic Activity ◽  
Satellite Cell ◽  
Muscle Development ◽  
Muscle Growth ◽  
Growth Potential ◽  
Unit Size ◽  
Skeletal Muscle Growth ◽  
Age Related ◽  
Related Increase

The role of satellite cells and DNA unit size in determining skeletal muscle growth was studied after mitotic activity was inhibited in the left pectoralis thoracicus of 2-wk-old tom turkeys by means of a 25-Gy dose of irradiation. Toms were killed and muscle weights were obtained 1 (n = 5), 4 (n = 6), 7 (n = 6), and 15 (n = 4) wk after irradiation. Satellite cell mitotic activity and DNA unit size were determined using enzymatically isolated myofiber segments and image analysis. Irradiated and nonirradiated muscle weights increased (P < 0.01) between all ages examined, but irradiated muscle weights were significantly (P < 0.01) lower than nonirradiated muscle weights at 4, 7, and 15 wk after irradiation. Satellite cell mitotic activity was lower (P < 0.01) in irradiated than in nonirradiated muscles at 1 and 4 wk after irradiation and resulted in a significant reduction (P < 0.05) in the number of myofiber nuclei per millimeter at 4 and 7 wk after irradiation. Satellite cell mitotic activity was higher (P < 0.05) in irradiated than in nonirradiated muscles at 7 wk after irradiation, but at 15 wk after irradiation it had fallen to low levels in both muscles. There was no significant (P > 0.10) difference in DNA unit size between muscles at any time, but there was an age-related increase (P < 0.01) for both muscles. Irradiation reduced muscle growth through a transient reduction in myonuclear production at a critical time (3-6 wk of age) in posthatch skeletal muscle development. The age-related increase in DNA unit size was not accelerated to compensate for the reduction in myonuclear accretion. Thus it appears that muscle growth potential is governed mostly by myonuclear accretion and to a lesser extent by DNA unit size.

scholarly journals Age-Related Exosomal and Endogenous Expression Patterns of miR-1, miR-133a, miR-133b, and miR-206 in Skeletal Muscles

2021 ◽  
Vol 12 ◽  
Author(s):  
Chrystalla Mytidou ◽  
Andrie Koutsoulidou ◽  
Margarita Zachariou ◽  
Marianna Prokopi ◽  
Konstantinos Kapnisis ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Skeletal Muscles ◽  
Connexin 43 ◽  
Muscle Development ◽  
Serum Response Factor ◽  
Expression Patterns ◽  
Muscle Growth ◽  
Skeletal Muscle Growth ◽  
Endogenous Expression ◽  
Age Related

Skeletal muscle growth and maintenance depend on two tightly regulated processes, myogenesis and muscle regeneration. Both processes involve a series of crucial regulatory molecules including muscle-specific microRNAs, known as myomiRs. We recently showed that four myomiRs, miR-1, miR-133a, miR-133b, and miR-206, are encapsulated within muscle-derived exosomes and participate in local skeletal muscle communication. Although these four myomiRs have been extensively studied for their function in muscles, no information exists regarding their endogenous and exosomal levels across age. Here we aimed to identify any age-related changes in the endogenous and muscle-derived exosomal myomiR levels during acute skeletal muscle growth. The four endogenous and muscle-derived myomiRs were investigated in five skeletal muscles (extensor digitorum longus, soleus, tibialis anterior, gastrocnemius, and quadriceps) of 2-week–1-year-old wild-type male mice. The expression of miR-1, miR-133a, and miR-133b was found to increase rapidly until adolescence in all skeletal muscles, whereas during adulthood it remained relatively stable. By contrast, endogenous miR-206 levels were observed to decrease with age in all muscles, except for soleus. Differential expression of the four myomiRs is also inversely reflected on the production of two protein targets; serum response factor and connexin 43. Muscle-derived exosomal miR-1, miR-133a, and miR-133b levels were found to increase until the early adolescence, before reaching a plateau phase. Soleus was found to be the only skeletal muscle to release exosomes enriched in miR-206. In this study, we showed for the first time an in-depth longitudinal analysis of the endogenous and exosomal levels of the four myomiRs during skeletal muscle development. We showed that the endogenous expression and extracellular secretion of the four myomiRs are associated to the function and size of skeletal muscles as the mice age. Overall, our findings provide new insights for the myomiRs’ significant role in the first year of life in mice.

Chapter 5 Role of cytokines in skeletal muscle growth and differentiation

2002 ◽  
pp. 97-126
Author(s):  
B.B. Olwin ◽  
Y. Bren-Mattison ◽  
D.D.W. Cornelison ◽  
Y.V. Fedorov ◽  
H. Flanagan-Steet ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Growth ◽  
Skeletal Muscle Growth

scholarly journals Circadian clock regulation of skeletal muscle growth and repair

F1000Research ◽  
2016 ◽  
Vol 5 ◽  
pp. 1549 ◽  
Author(s):  
Somik Chatterjee ◽  
Ke Ma
Keyword(s):  
Skeletal Muscle ◽  
Circadian Clock ◽  
Muscle Growth ◽  
Muscle Metabolism ◽  
Muscle Physiology ◽  
Skeletal Muscle Growth ◽  
Age Related ◽  
Evolutionarily Conserved ◽  
Key Aspects ◽  
And Function

Accumulating evidence indicates that the circadian clock, a transcriptional/translational feedback circuit that generates ~24-hour oscillations in behavior and physiology, is a key temporal regulatory mechanism involved in many important aspects of muscle physiology. Given the clock as an evolutionarily-conserved time-keeping mechanism that synchronizes internal physiology to environmental cues, locomotor activities initiated by skeletal muscle enable entrainment to the light-dark cycles on earth, thus ensuring organismal survival and fitness. Despite the current understanding of the role of molecular clock in preventing age-related sarcopenia, investigations into the underlying molecular pathways that transmit clock signals to the maintenance of skeletal muscle growth and function are only emerging. In the current review, the importance of the muscle clock in maintaining muscle mass during development, repair and aging, together with its contribution to muscle metabolism, will be discussed. Based on our current understandings of how tissue-intrinsic muscle clock functions in the key aspects muscle physiology, interventions targeting the myogenic-modulatory activities of the clock circuit may offer new avenues for prevention and treatment of muscular diseases. Studies of mechanisms underlying circadian clock function and regulation in skeletal muscle warrant continued efforts.

Role of Satellite Cells in FoxO1-Mediated Skeletal Muscle Growth

2007 ◽  
Vol 39 (Supplement) ◽  
pp. S223
Author(s):  
Alissa DeLong ◽  
Yasutomi Kamei ◽  
Shinji Miura ◽  
Osamu Ezaki ◽  
Thomas J. McLoughlin
Keyword(s):  
Skeletal Muscle ◽  
Satellite Cells ◽  
Muscle Growth ◽  
Skeletal Muscle Growth
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