Bio-chemo-mechanical coupling models of soft biological materials: A review

Sun, Shu-Yi; Zhang, Huanxin; Fang, Wei; Chen, Xindong; Li, Bo; Feng, Xi‐Qiao

doi:10.1016/bs.aams.2022.05.004

Cited by 12 publications

(3 citation statements)

References 312 publications

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“…Another model demonstrated how the interaction between cells and ECM affects both gene expression and nuclear architecture [ 101 ]. This group of models is reviewed in [ 102 , 103 ].…”

Section: Active Contractile Elementsmentioning

confidence: 99%

Active viscoelastic models for cell and tissue mechanics

Tajvidi Safa,

Huang,

Kabla

et al. 2024

R. Soc. Open Sci.

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Living cells are out of equilibrium active materials. Cell-generated forces are transmitted across the cytoskeleton network and to the extracellular environment. These active force interactions shape cellular mechanical behaviour, trigger mechano-sensing, regulate cell adaptation to the microenvironment and can affect disease outcomes. In recent years, the mechanobiology community has witnessed the emergence of many experimental and theoretical approaches to study cells as mechanically active materials. In this review, we highlight recent advancements in incorporating active characteristics of cellular behaviour at different length scales into classic viscoelastic models by either adding an active tension-generating element or adjusting the resting length of an elastic element in the model. Summarizing the two groups of approaches, we will review the formulation and application of these models to understand cellular adaptation mechanisms in response to various types of mechanical stimuli, such as the effect of extracellular matrix properties and external loadings or deformations.

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“…Another model demonstrated how the interaction between cells and ECM affects both gene expression and nuclear architecture [ 101 ]. This group of models is reviewed in [ 102 , 103 ].…”

Section: Active Contractile Elementsmentioning

confidence: 99%

Active viscoelastic models for cell and tissue mechanics

Tajvidi Safa,

Huang,

Kabla

et al. 2024

R. Soc. Open Sci.

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“…Cells are able to sense the physical properties of the extracellular matrices (ECMs), such as stiffness , and viscoelasticity, − through integrin-containing adhesion complexes. It is well recognized that cell spreading, migration, proliferation, and cell differentiation are regulated by the mechanical properties of ECMs. − This mechanosensing capability of cells is primarily attributed to the force-sensitive receptors (such as integrin, vinculin, and talin) of adhesion complexes. − The adhesion complexes, acting like molecule clutches, can get dynamically stretched by the actin retrograde flow generated by the pulling forces of intracellular myosin . By gauging the forces sustained by adhesion complexes, cells can translate mechanical signals into biochemical signals via mechanotransduction, which in turn governs their behaviors to accommodate alterations in the external stimuli.…”

mentioning

confidence: 99%

Superposition of Substrate Deformation Fields Induced by Molecular Clutches Explains Cell Spatial Sensing of Ligands

Xue,

Chen,

Gong

et al. 2024

ACS Nano

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Cells can sense the physical properties of the extracellular matrices (ECMs), such as stiffness and ligand density, through cell adhesions to actively regulate their behaviors. Recent studies have shown that varying ligand spacing of ECMs can influence adhesion size, cell spreading, and even stem cell differentiation, indicating that cells have the spatial sensing ability of ECM ligands. However, the mechanism of the cells' spatial sensing remains unclear. In this study, we have developed a lattice-spring motor-clutch model by integrating cell membrane deformation, the talin unfolding mechanism, and the lattice spring for substrate ligand distribution to explore how the spatial distribution of integrin ligands and substrate stiffness influence cell spreading and adhesion dynamics. By applying the Gillespie algorithm, we found that large ligand spacing reduces the superposition effect of the substrate's displacement fields generated by pulling force from motor-clutch units, increasing the effective stiffness probed by the force-sensitive receptors; this finding explains a series of previous experiments. Furthermore, using the mean-field theory, we obtain the effective stiffness sensed by bound clutches analytically; our analysis shows that the bound clutch number and ligand spacing are the two key factors that affect the superposition effects of deformation fields and, hence, the effective stiffness. Overall, our study reveals the mechanism of cells' spatial sensing, i.e., ligand spacing changes the effective stiffness sensed by cells due to the superposition effect of deformation fields, which provides a physical clue for designing and developing biological materials that effectively control cell behavior and function.

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“…Constructing a predictive spatiotemporal multiscale modeling system that can describe cellular dynamic behaviors from the molecular proteins at the intersection of biology, physics, chemistry, and computer science will greatly accelerate biomedical advancements ( 34 , 35 ). From the level of protein–protein interactions, we here derive a spatiotemporal “resistance- daptive propulsion” (RAP) theory based on the geometric nonlinear deformation mechanisms of polymerizing actin filaments and the mechano-chemical assembling behaviors of Arp2/3 complexes.…”

mentioning

confidence: 99%

Polymerization force–regulated actin filament–Arp2/3 complex interaction dominates self-adaptive cell migrations

Chen,

Li,

Guo

et al. 2023

Proc. Natl. Acad. Sci. U.S.A.

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Cells migrate by adapting their leading-edge behaviors to heterogeneous extracellular microenvironments (ECMs) during cancer invasions and immune responses. Yet it remains poorly understood how such complicated dynamic behaviors emerge from millisecond-scale assembling activities of protein molecules, which are hard to probe experimentally. To address this gap, we establish a spatiotemporal “resistance-adaptive propulsion” theory based on the interactions between Arp2/3 complexes and polymerizing actin filaments and a multiscale dynamic modeling system spanning from molecular proteins to the cell. We quantitatively find that cells can accurately self-adapt propulsive forces to overcome heterogeneous ECMs via a resistance-triggered positive feedback mechanism, dominated by polymerization-induced actin filament bending and the bending-regulated actin-Arp2/3 binding. However, for high resistance regions, resistance triggers a negative feedback, hindering branched filament assembly, which adapts cellular morphologies to circumnavigate the obstacles. Strikingly, the synergy of the two opposite feedbacks not only empowers the cell with both powerful and flexible migratory capabilities to deal with complex ECMs but also enables efficient utilization of intracellular proteins by the cell. In addition, we identify that the nature of cell migration velocity depending on ECM history stems from the inherent temporal hysteresis of cytoskeleton remodeling. We also show that directional cell migration is dictated by the competition between the local stiffness of ECMs and the local polymerizing rate of actin network caused by chemotactic cues. Our results reveal that it is the polymerization force–regulated actin filament–Arp2/3 complex binding interaction that dominates self-adaptive cell migrations in complex ECMs, and we provide a predictive theory and a spatiotemporal multiscale modeling system at the protein level.

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Bio-chemo-mechanical coupling models of soft biological materials: A review

Cited by 12 publications

References 312 publications

Active viscoelastic models for cell and tissue mechanics

Active viscoelastic models for cell and tissue mechanics

Superposition of Substrate Deformation Fields Induced by Molecular Clutches Explains Cell Spatial Sensing of Ligands

Polymerization force–regulated actin filament–Arp2/3 complex interaction dominates self-adaptive cell migrations

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