ArticleCommunications materials2024
Myosin-independent stiffness sensing by fibroblasts is regulated by the viscoelasticity of flowing actin.
Article in Communications materials, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
11 citing papers in PubMed.
- Single Cell Mechanics in Disease Progression.Small science · 2026Review
- Hydrostatic pressure reduces the mechanosensitivity of cell migration.Science advances · 2026Article
- Cell loss disrupts mechanical homeostasis to drive retinal pigment epithelium ageing-like phenotype in vitro.Nature communications · 2026Article
- Physiomimetic culture bias durotaxis toward soft environments.bioRxiv : the preprint server for biology · 2026Article
- Regulated RIAM-Talin Engagement Controls Adhesion Stability and Mechanical Output.bioRxiv : the preprint server for biology · 2026Article
- The role of extracellular matrix stiffness in regulating fibroblast behaviors and disease progression.Frontiers in immunology · 2026Review
- Aligned Collagen Fibers Drive Distinct Traction Force Signatures to Regulate Contact Guidance.ACS nano · 2025Article
- How Actin Polymerization and Myosin II Activity Regulate Focal Adhesion Dynamics in Motile Cells.International journal of molecular sciences · 2025Article
- The PAX3-FOXO1 fusion gene reduces cell-ECM interactions and TGFβ signaling in rhabdomyosarcoma.The Journal of cell biology · 2025Article
- TRPV4 Dominates High Shear-Induced Initial Traction Response and Long-Term Relaxation Over Piezo1.bioRxiv : the preprint server for biology · 2025Article
- Transient low shear-stress preconditioning influences long-term endothelial traction and alignment under high shear flow.American journal of physiology. Heart and circulatory physiology · 2024Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
The stiffness of the extracellular matrix induces differential tension within integrin-based adhesions, triggering differential mechanoresponses. However, it has been unclear if the stiffness-dependent differential tension is induced solely by myosin activity. Here, we report that in the absence of myosin contractility, 3T3 fibroblasts still transmit stiffness-dependent differential levels of traction. This myosin-independent differential traction is regulated by polymerizing actin assisted by actin nucleators Arp2/3 and formin where formin has a stronger contribution than Arp2/3 to both traction and actin flow. Intriguingly, despite only slight changes in F-actin flow speed observed in cells with the combined inhibition of Arp2/3 and myosin compared to cells with sole myosin inhibition, they show a 4-times reduction in traction than cells with myosin-only inhibition. Our analyses indicate that traditional models based on rigid F-actin are inadequate for capturing such dramatic force reduction with similar actin flow. Instead, incorporating the F-actin network's viscoelastic properties is crucial. Our new model including the F-actin viscoelasticity reveals that Arp2/3 and formin enhance stiffness sensitivity by mechanically reinforcing the F-actin network, thereby facilitating more effective transmission of flow-induced forces. This model is validated by cell stiffness measurement with atomic force microscopy and experimental observation of model-predicted stiffness-dependent actin flow fluctuation.
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.