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.

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).

Satellite cell proliferation and differentiation during postnatal growth of porcine skeletal muscle

2002 ◽  
Vol 282 (4) ◽  
pp. C899-C906 ◽  
Author(s):  
N. T Mesires ◽  
M. E. Doumit
Keyword(s):  
Skeletal Muscle ◽  
Cell Proliferation ◽  
Satellite Cell ◽  
Satellite Cells ◽  
Nuclear Antigen ◽  
Positive Staining ◽  
Age Related ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation ◽  
Satellite Cell Proliferation

Age-related changes in satellite cell proliferation and differentiation during rapid growth of porcine skeletal muscle were examined. Satellite cells were isolated from hindlimb muscles of pigs at 1, 7, 14, and 21 wk of age (4 animals/age group). Satellite cells were separated from cellular debris by using Percoll gradient centrifugation and were adsorbed to glass coverslips for fluorescent immunostaining. Positive staining for neural cell adhesion molecule (NCAM) distinguished satellite cells from nonmyogenic cells. The proportion of NCAM-positive cells (satellite cells) in isolates decreased from 1 to 7 wk of age. Greater than 77% of NCAM-positive cells were proliferating cell nuclear antigen positive at all ages studied. Myogenin-positive satellite cells decreased from 30% at 1 wk to 14% at 7 wk of age and remained at constant levels thereafter. These data indicate that a high percentage of satellite cells remain proliferative during rapid postnatal muscle growth. The reduced proportion of myogenin-positive cells during growth may reflect a decrease in the proportion of differentiating satellite cells or accelerated incorporation of myogenin-positive cells into myofibers.

004.Control of skeletal muscle cell proliferation and differentiation

2005 ◽  
Vol 17 (9) ◽  
pp. 63
Author(s):  
M. Grounds
Keyword(s):  
Skeletal Muscle ◽  
Cell Proliferation ◽  
Multinucleated Cells ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation ◽  
The Matrix ◽  
Key Issues

Skeletal muscle is formed by mononucleated precursor cells (myoblasts) that cease cell proliferation to start differentiation; this results in fusion between the myoblasts to form multinucleated cells (myotubes) that continue to differentiate (and fuse with more muscle cells) and mature into myofibres. Myogenesis has been widely used as a model to study in vitro factors controlling cell proliferation and differentiation. Condition in vitro may not reflect what happens in the more complex in vivo environment. Some of the key issues are what activates quiescent myoblasts in mature skeletal muscle in vivo, and what controls the switch between proliferation and differentiation? The role of the matrix, and molecules such as MyoD, p53, NFAT and IGF-1 will be considered.

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