Search for: All records

When adherent cells are subjected to uniaxial sinusoidal stretch at frequencies close to physiological, their body and their contractile stress fibers realign nearly perpendicularly to the stretch axis. A common explanation for this phenomenon is that stress fibers reorient along the direction where they are unaffected by the applied cyclic stretch and thus can maintain optimal (homeostatic) tensile force. The ability of cells to achieve tensional homeostasis in response to external disturbances is important for normal physiological functions of cells and tissues and it provides protection against diseases, including cancer and atherosclerosis. However, quantitative experimental data that support the idea that stretch-induced reorientation is associated with tensional homeostasis are lacking. We observed previously that in response to uniaxial cyclic stretch of 10% strain amplitudes, traction forces of single endothelial cells reorient in the direction perpendicular to the stretch axis. Here we carried out a secondary analysis of those data to investigate whether this reorientation of traction forces is associated with tensional homeostasis. Our analysis showed that stretch-induced reorientation of traction forces was accompanied by attenuation of temporal variability of the traction field to the level that was observed in the absence of stretch. These findings represent a quantitative experimental evidence that stretch-induced reorientation of the cell’s traction forces is associated with the cell’s tendency to achieve tensional homeostasis. 

The ability of cells to maintain a constant level of cytoskeletal tension in response to external and internal disturbances is referred to as tensional homeostasis. It is essential for the normal physiological function of cells and tissues, and for protection against disease progression, including atherosclerosis and cancer. In previous studies, we defined tensional homeostasis as the ability of cells to maintain a consistent level of cytoskeletal tension with low temporal fluctuations. In those studies, we measured temporal fluctuations of cell-substrate traction forces in clusters of endothelial cells and of fibroblasts. We observed those temporal fluctuations to decrease with increasing cluster size in endothelial cells, but not in fibroblasts. We quantified temporal fluctuation, and thus homeostasis, through the coefficient of variation (CV) of the traction field; the lower the value of CV, the closer the cell is to the state of tensional homeostasis. This metric depends on correlation between individual traction forces. In this study, we analyzed the contribution of correlation between traction forces on traction field CV in clusters of endothelial cells and fibroblasts using experimental data that we had obtained previously. Results of our analysis showed that positive correlation between traction forces was detrimental to homeostasis, and that it was cell type-dependent.