Towards the understanding of cytoskeleton fluidisation–solidification regulation

• Published in: Biomechanics and modeling in mechanobiology Vol. 16; no. 4; pp. 1159 - 1169
• Main Authors: López-Menéndez, Horacio, Rodríguez, José Félix
• Format: Journal Article
• Language: English
• Published: Berlin/Heidelberg Springer Berlin Heidelberg 01.08.2017; Springer Nature B.V
• Subjects: Actinin; Actinin - metabolism; Actins - metabolism; Biological and Medical Physics; Biomechanics; Biomedical Engineering and Bioengineering; Biophysics; Cells; Complexity; Contractility; Coupling (molecular); Crosslinking; Crosstalk; Cytoskeleton; Cytoskeleton - physiology; Elasticity; Engineering; Fluid mechanics; Gelation; Links; Lungs; Mechanical properties; Mechanics (physics); Models, Biological; Molecular motors; Molecular structure; Myosin; Myosins - metabolism; Original Paper; Signal transduction; Signaling; Solidification; Space life sciences; Stress relaxation; Theoretical and Applied Mechanics; Crosslinks; Prestress; Non-sarcomeric cells; F-actin networks; Fluidisation-solidification
• ISSN: 1617-7959; 1617-7940
• DOI: 10.1007/s10237-017-0878-6

The understanding of the self-regulation of the mechanical properties in non-sarcomeric cells, such as lung cells or cells during tissue development, remains an open research problem with many unresolved issues. Their behaviour is far from the image of the traditionally studied sarcomeric cells, since the crosstalk between the signalling pathways and the complexity of the mechanical properties creates an intriguing mechano-chemical coupling. In these situations, the inelastic effects dominate the cytoskeletal structure showing phenomena like fluidisation and subsequent solidification. Here, we proposes the inelastic contractile unit framework as an attempt to reconciles these effects. The model comprises a mechanical description of the nonlinear elasticity of the cytoskeleton incorporated into a continuum-mechanics framework using the eighth-chains model. In order to address the inelastic effect, we incorporate the dynamic of crosslinks, considering the α -actinin and the active stress induced by the myosin molecular motors. Finally, we introduce a hypothesis that links the ability to fluidise and re-solidify as a consequence of the interaction between the active stress and the gelation state defined by the crosslinks. We validate the model with data obtained from experiments of drug-induced relaxation reported in the literature.