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Updated: Oct 3, 2025

Chondrogenic Differentiation Induction of Adipose-derived Stem Cells by Centrifugal Gravity
Published on: February 24, 2017
Chondroitin sulfate E downregulates N-cadherin and suppresses myotube formation
Fumi Satoh1, Akihiro Sugiura1, Jiro Tashiro1
1Department of Veterinary Anatomy, Faculty of Agriculture, Tottori University, Tottori, Japan.
Abstract:
Myogenesis, the formation of muscle fibers, is affected by certain glycoproteins, including chondroitin sulfate (CS), which are involved in various cellular processes. We aimed to investigate the mechanism underlying CS-E-induced suppression of myotube formation using the myoblast cell line C2C12. Differentiated cells treated with 0.1 mg/ml CS-E for nine days showed multinucleated and rounded myotubes with myosin heavy chain positivity. No difference was found between the CS-E-treated group with rounded myotubes and CS (-) controls with elongated myotubes in the levels of phospho-cofilin, a protein involved in the dynamics of actin cytoskeleton. Interestingly, N-cadherin, which is involved in the gene expression of myoblast fusion factors (myomaker and myomixer), was significantly downregulated at both the mRNA and protein levels following CS-E treatment. These results suggest that N-cadherin downregulation is one of the mechanisms underlying the CS-E-induced suppression of myotube formation.
Insights
Chondroitin sulfate-E (CS-E) inhibits muscle fiber formation by downregulating N-cadherin. This protein is crucial for myoblast fusion, suggesting a new mechanism for impaired myogenesis.
Area of Science:
- Biochemistry
- Cell Biology
- Molecular Biology
Background:
- Myogenesis, the process of muscle fiber formation, is essential for muscle development and repair.
- Glycoproteins like chondroitin sulfate (CS) play regulatory roles in cellular processes, including myogenesis.
- Specific CS modifications, such as CS-E, may influence myoblast differentiation and fusion.
Purpose of the Study:
- To elucidate the molecular mechanism by which CS-E suppresses myotube formation.
- To investigate the role of N-cadherin in CS-E-mediated inhibition of myogenesis.
Main Methods:
- Utilized the C2C12 myoblast cell line for in vitro studies.
- Treated differentiated myoblasts with CS-E (0.1 mg/ml) for nine days.
- Assessed myotube morphology, myosin heavy chain expression, phospho-cofilin levels, and N-cadherin expression at both mRNA and protein levels.
Main Results:
- CS-E treatment resulted in rounded, multinucleated myotubes positive for myosin heavy chain.
- Phospho-cofilin levels did not differ between CS-E treated and control groups.
- N-cadherin expression was significantly downregulated at both mRNA and protein levels in response to CS-E treatment.
Conclusions:
- CS-E significantly inhibits myotube formation in C2C12 cells.
- Downregulation of N-cadherin is identified as a key mechanism underlying CS-E-induced suppression of myogenesis.
- These findings highlight N-cadherin's critical role in myoblast fusion and its potential as a target for modulating muscle formation.
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