ArticleBiophysical journal2017
Mutation in the Core Structure of Desmin Intermediate Filaments Affects Myoblast Elasticity.
Article in Biophysical journal, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- Viscoelasticity of the Heart: An Overview of Viscoelastic Measurements at Different Scales.Annual review of biomedical engineering · 2026Review
- Chaperone proteins protect against desmin fragment amyloid aggregation.Biophysical journal · 2026Article
- Common and Key Differential Pathogenic Pathways in Desminopathy and Titinopathy.International journal of medical sciences · 2024Article
- Desmin mutations impact the autophagy flux in C2C12 cell in mutation-specific manner.Cell and tissue research · 2023Article
- The importance of intermediate filaments in the shape maintenance of myoblast model tissues.eLife · 2022Article
- Expression patterns and correlation analyses of muscle-specific genes in the process of sheep myoblast differentiation.In vitro cellular & developmental biology. Animal · 2022Article
- Molecular insights into cardiomyopathies associated with desmin (DES) mutations.Biophysical reviews · 2018Review
Corrections and comments
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Authors and funding
10 authors at 7 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Elastic properties of cells are mainly derived from the actin cytoskeleton. However, intermediate filaments are emerging as major contributors to the mechanical properties of cells. Using atomic force microscopy, we studied the elasticity of mouse myoblasts expressing a mutant form of the gene encoding for desmin intermediate filaments, p.D399Y. This variant produces desmin aggregates, the main pathological symptom of myofibrillar myopathies. Here we show that desmin-mutated cells display a 39% increased median elastic modulus compared to wild-type cells. Desmin-mutated cells required higher forces than wild-type cells to reach high indentation depths, where desmin intermediate filaments are typically located. In addition, heat-shock treatment increased the proportion of cells with aggregates and induced a secondary peak in the distribution of Young's moduli. By performing atomic force microscopy mechanical mapping combined with fluorescence microscopy, we show that higher Young's moduli were measured where desmin aggregates were located, indicating that desmin aggregates are rigid. Therefore, we provide evidence that p.D399Y stiffens mouse myoblasts. Based on these results, we suggest that p.D399Y-related myofibrillar myopathy is at least partly due to altered mechanical properties at the single-cell scale, which are propagated to the tissue scale.
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Registered trials
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