The role of transmembrane proteins on force transmission in skeletal muscle

Zhang, Chi; Gao, Yingxin

doi:10.1016/j.jbiomech.2014.07.014

Cited by 7 publications

(8 citation statements)

References 28 publications

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“…Our predictions are consistent with recent studies which determined the influence of transmembrane protein density and stiffness on lateral force transmission [30]. Supporting that study, we found that the stiffness of the protein had minimal effect on the fascicle shear modulus, while the density of proteins significantly affected the fascicle shear modulus.…”

Section: Discussionsupporting

confidence: 93%

“…Indeed, increasing the volume fraction of ECM could be paired with changes in collagen content and architecture, which would also influence the tissue-level properties and potential damage sensitivity of the membrane. Further, the mechanical properties of the transmembrane proteins were represented using a continuous nonlinear curve [30], although physiological models often represent it as a piecewise function due to the unfolding of the protein [31,32].…”

Section: Discussionmentioning

confidence: 99%

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Multiscale models of skeletal muscle reveal the complex effects of muscular dystrophy on tissue mechanics and damage susceptibility

et al. 2015

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Computational models have been increasingly used to study the tissue-level constitutive properties of muscle microstructure; however, these models were not created to study or incorporate the influence of disease-associated modifications in muscle. The purpose of this paper was to develop a novel multiscale muscle modelling framework to elucidate the relationship between microstructural disease adaptations and modifications in both mechanical properties of muscle and strain in the cell membrane. We used an agent-based model to randomly generate new muscle fibre geometries and mapped them into a finite-element model representing a cross section of a muscle fascicle. The framework enabled us to explore variability in the shape and arrangement of fibres, as well as to incorporate disease-related changes. We applied this method to reveal the trade-offs between mechanical properties and damage susceptibility in Duchenne muscular dystrophy (DMD). DMD is a fatal genetic disease caused by a lack of the transmembrane protein dystrophin, leading to muscle wasting and death due to cardiac or pulmonary complications. The most prevalent microstructural variations in DMD include: lack of transmembrane proteins, fibrosis, fatty infiltration and variation in fibre cross-sectional area. A parameter analysis of these variations and case study of DMD revealed that the nature of fibrosis and density of transmembrane proteins strongly affected the stiffness of the muscle and susceptibility to membrane damage.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Multiscale models of skeletal muscle reveal the complex effects of muscular dystrophy on tissue mechanics and damage susceptibility

et al. 2015

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“…Indeed, disorganization of sarcomeres due to the lack or presence of desmin aggregates generates a defect in force production ( Li et al, 1997 ; Anderson et al, 2002 ) that causes the muscle weakness observed in patients. However, force transmission is not only longitudinal to the tendon ( Sharafi and Blemker, 2011 ), but also lateral from costameres to the endomysium ( Zhang and Gao, 2014 ). Thus, reduced force production and altered force transmission would generate significant muscle weakness in patients.…”

Section: Discussionmentioning

confidence: 99%

Desmin Modulates Muscle Cell Adhesion and Migration

Hakibilen

Delort

Daher

et al. 2022

Front. Cell Dev. Biol.

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Cellular adhesion and migration are key functions that are disrupted in numerous diseases. We report that desmin, a type-III muscle-specific intermediate filament, is a novel cell adhesion regulator. Expression of p.R406W mutant desmin, identified in patients with desmin-related myopathy, modified focal adhesion area and expression of adhesion-signaling genes in myogenic C2C12 cells. Satellite cells extracted from desmin-knock-out (DesKO) and desmin-knock-in-p.R405W (DesKI-R405W) mice were less adhesive and migrated faster than those from wild-type mice. Moreover, we observed mislocalized and aggregated vinculin, a key component of cell adhesion, in DesKO and DesKI-R405W muscles. Vinculin expression was also increased in desmin-related myopathy patient muscles. Together, our results establish a novel role for desmin in cell-matrix adhesion, an essential process for strength transmission, satellite cell migration and muscle regeneration. Our study links the patho-physiological mechanisms of desminopathies to adhesion/migration defects, and may lead to new cellular targets for novel therapeutic approaches.

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“…Nevertheless, the cell response is also dependent on the contractile forces present in the intracellular matrix of the cell. The mechanotransduction process is regulated by the cross-talk between ECM and ICM, implying different transmembrane proteins, such as dystroglycan, sarcoglycans or intergrins, for instance [ 78 , 147 , 148 ]. For the striated muscle cells, the mechanical cross is mainly between ECM and ICM in the skeletal muscle, while in the heart, there is an additional cross-talk between the cells.…”

Section: Muscle Lim Proteinmentioning

confidence: 99%

Role of Muscle LIM Protein in Mechanotransduction Process

Germain

Delalande

Pichon

2022

IJMS

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The induction of protein synthesis is crucial to counteract the deconditioning of neuromuscular system and its atrophy. In the past, hormones and cytokines acting as growth factors involved in the intracellular events of these processes have been identified, while the implications of signaling pathways associated with the anabolism/catabolism ratio in reference to the molecular mechanism of skeletal muscle hypertrophy have been recently identified. Among them, the mechanotransduction resulting from a mechanical stress applied to the cell appears increasingly interesting as a potential pathway for therapeutic intervention. At present, there is an open question regarding the type of stress to apply in order to induce anabolic events or the type of mechanical strain with respect to the possible mechanosensing and mechanotransduction processes involved in muscle cells protein synthesis. This review is focused on the muscle LIM protein (MLP), a structural and mechanosensing protein with a LIM domain, which is expressed in the sarcomere and costamere of striated muscle cells. It acts as a transcriptional cofactor during cell proliferation after its nuclear translocation during the anabolic process of differentiation and rebuilding. Moreover, we discuss the possible opportunity of stimulating this mechanotransduction process to counteract the muscle atrophy induced by anabolic versus catabolic disorders coming from the environment, aging or myopathies.

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The role of transmembrane proteins on force transmission in skeletal muscle

Cited by 7 publications

References 28 publications

Multiscale models of skeletal muscle reveal the complex effects of muscular dystrophy on tissue mechanics and damage susceptibility

Multiscale models of skeletal muscle reveal the complex effects of muscular dystrophy on tissue mechanics and damage susceptibility

Desmin Modulates Muscle Cell Adhesion and Migration

Role of Muscle LIM Protein in Mechanotransduction Process

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