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Resistance exercise and mechanical overload upregulate vimentin for skeletal muscle remodeling
Joshua S Godwin1, J Max Michel1, Cleiton A Libardi2
1Nutrabolt Applied and Molecular Physiology Laboratory, School of Kinesiology, Auburn University, Auburn, Alabama, United States.
American Journal of Physiology. Cell Physiology
|April 3, 2025
Summary
Mechanical overload (MOV) increases skeletal muscle vimentin (VIM) in the extracellular matrix (ECM). Satellite cells may regulate VIM, and disrupted VIM during MOV leads to excessive muscle regeneration.
Area of Science:
- Muscle physiology and mechanobiology
- Proteomics and molecular biology
Background:
- Skeletal muscle adaptation to mechanical overload (MOV) involves complex molecular responses.
- Understanding novel targets and regulatory mechanisms is crucial for muscle health and performance.
Purpose of the Study:
- To investigate the role of mechanical overload (MOV) on novel skeletal muscle targets.
- To explore how perturbations in adaptive responses, specifically vimentin (VIM) expression, affect skeletal muscle adaptation.
- To determine the cellular origins and functional consequences of VIM enrichment in the extracellular matrix (ECM) following MOV.
Main Methods:
- Proteomic analysis of sarcolemmal proteins following 10 weeks of resistance training in college-aged females.
- Mass spectrometry to identify upregulated proteins, focusing on vimentin (VIM).
- In vivo studies in mice using plantaris muscle synergist ablation models to induce MOV, examining VIM expression via mRNA, protein, and immunohistochemistry.
- Experiments utilizing Pax7-DTA mice (satellite cell depleted) and AAV9-VIM-shRNA to investigate VIM regulation and functional impact.
Main Results:
- Resistance training increased sarcolemmal-associated protein content, with ~10% of identified proteins upregulated, including vimentin (VIM).
- VIM mRNA and protein levels were significantly elevated in mouse plantaris muscle following MOV, primarily localized to the ECM.
- Satellite cell depletion reduced ECM VIM, and VIM knockdown via shRNA did not alter muscle mass gain but resulted in smaller, more centrally nucleated fibers, indicating an altered regenerative phenotype.
Conclusions:
- Skeletal muscle vimentin (VIM) is enriched in the extracellular matrix (ECM) following mechanical overload (MOV).
- Satellite cells appear to play a role in regulating VIM expression in the ECM during MOV.
- Dysregulation of VIM during MOV leads to an exaggerated regenerative response, suggesting VIM's role in tissue remodeling and adaptation.
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