Using matrices of varying stiffness and measurements of endothelial cell migration and traction stresses, we find that cells can detect and respond to substrate strains created by the traction stresses of a neighboring cell, and that this response is dependent on matrix stiffness.
Using an array of micron-sized pillars as a force sensor and shRNA specific to each myosin II isoform (A and B), we analyzed how myosin IIA and IIB individually regulate cell migration and traction force generation.
Accordingly, we based the current study on fibroblasts derived from rabbit fetal and adult skin and focused on the role of CCT-eta in fibroblast migration and cellular traction force, two key determinants of the fibrotic phase of dermal repair.
Cancer cell interactions with the extracellular matrix and the migration therein require adhesion and traction provided by integrins, together with pericellular proteolysis executed by extracellular matrix degrading proteases.
Even though inflammation is based on the recruitment of individual neutrophils to the site of wounding or infection – and not coordinated and cohesive collective cell migration – in both individual and collective cell migration, cells need adhesion to, and traction on, the substratum, and progress through the extracellular matrix driven by distant guidance signals.
Again however, the process is complex and is due both to contraction in the surrounding matrix, in the same way as a sea anemone retracts its tentacles, and traction or migration of fibroblasts through surrounding matrix, akin to the movement of a spider through its web, pulling on the filaments.
It is suggested that TNC produced by interstitial cells at an early phase of myocardial infarction promotes recruitment of myofibroblasts to injured sites by accelerating migration and differentiation and enhancing traction forces [25].
Like most migrating cells, border cells normally extend and retract actin-rich cellular protrusions that provide traction for migration and help them sense directional guidance cues (Murphy and Montell 1996; Fulga and Rørth 2002; Prasad and Montell 2007).
Wolf, K. et al. Physical limits of cell migration: Control by ECM space and nuclear deformation and tuning by proteolysis and traction force.
For this purpose, we carried out simultaneous measurements of the time evolution of cell shape and traction forces exerted by isolated Dictyostelium cells undergoing chemotactic migration over a flat elastic substrate.
Through cell migration, Ca2+ signaling is involved in the directional sensing of the cells, in the redistribution and traction force of the cytoskeleton and in the repositioning of new focal adhesions [ 22, 23].
