scholarly journals The effects of Capn1 gene inactivation on skeletal muscle growth, development, and atrophy, and the compensatory role of other proteolytic systems1

2013 ◽  
Vol 91 (7) ◽  
pp. 3155-3167 ◽  
Author(s):  
C. M. Kemp ◽  
W. T. Oliver ◽  
T. L. Wheeler ◽  
A. H. Chishti ◽  
M. Koohmaraie
Keyword(s):  
Skeletal Muscle ◽  
Muscle Growth ◽  
Gene Inactivation ◽  
Skeletal Muscle Growth ◽  
Growth Development

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.

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

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

scholarly journals Physiological role of Kvβ2 (AKR6) in murine skeletal muscle growth and regulation

2018 ◽  
Vol 224 (2) ◽  
pp. e13083 ◽  
Author(s):  
K. C. Chapalamadugu ◽  
J. Tur ◽  
S. L. Badole ◽  
R. C. Kukreja ◽  
M. Brotto ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Growth ◽  
Physiological Role ◽  
Skeletal Muscle Growth ◽  
Murine Skeletal Muscle

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.

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