ArticleBiophysical journal2016
Desmin Mutation in the C-Terminal Domain Impairs Traction Force Generation in Myoblasts.
Article in Biophysical journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 24 citations in OpenAlex.
- Common and Key Differential Pathogenic Pathways in Desminopathy and Titinopathy.International journal of medical sciences · 2024Article
- The importance of intermediate filaments in the shape maintenance of myoblast model tissues.eLife · 2022Article
- Desmin Modulates Muscle Cell Adhesion and Migration.Frontiers in cell and developmental biology · 2022Article
- May the force be with your (immune) cells: an introduction to traction force microscopy in Immunology.Frontiers in immunology · 2022Review
- Cell geometry and the cytoskeleton impact the nucleo-cytoplasmic localisation of the SMYD3 methyltransferase.Scientific reports · 2020Article
- Primary cilia control glucose homeostasis via islet paracrine interactions.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Cardiac Tissue Chips (CTCs) for Modeling Cardiovascular Disease.IEEE transactions on bio-medical engineering · 2019Article
- Actomyosin contractility scales with myoblast elongation and enhances differentiation through YAP nuclear export.Scientific reports · 2019Article
- Molecular insights into cardiomyopathies associated with desmin (DES) mutations.Biophysical reviews · 2018Review
- Mutation in the Core Structure of Desmin Intermediate Filaments Affects Myoblast Elasticity.Biophysical journal · 2017Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The cytoskeleton plays a key role in the ability of cells to both resist mechanical stress and generate force, but the precise involvement of intermediate filaments in these processes remains unclear. We focus here on desmin, a type III intermediate filament, which is specifically expressed in muscle cells and serves as a skeletal muscle differentiation marker. By using several complementary experimental techniques, we have investigated the impact of overexpressing desmin and expressing a mutant desmin on the passive and active mechanical properties of C2C12 myoblasts. We first show that the overexpression of wild-type-desmin increases the overall rigidity of the cells, whereas the expression of a mutated E413K desmin does not. This mutation in the desmin gene is one of those leading to desminopathies, a subgroup of myopathies associated with progressive muscular weakness that are characterized by the presence of desmin aggregates and a disorganization of sarcomeres. We show that the expression of this mutant desmin in C2C12 myoblasts induces desmin network disorganization, desmin aggregate formation, and a small decrease in the number and total length of stress fibers. We finally demonstrate that expression of the E413K mutant desmin also alters the traction forces generation of single myoblasts lacking organized sarcomeres.
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