Fig. 5.
Effect of the global architecture of the F-actin cytoskeleton (CSK) on cell shape-dependent endothelial mechanotransduction. Our experimental results and theoretical modeling suggested that cell shape, by modulating the global architecture of the F-actin CSK, could independently dictate the extent of EC mechanosensitive contractile and adhesion responses to uniaxial stretch, which might further determine downstream pro- or anti-inflammatory signaling activities in ECs. Our results suggested a direct feedback between EC morphology and cellular mechanoresponsiveness to external stretch, with non-polarized cell morphology primed for elevated EC responses leading to EC inflammation and polarized cell morphology with the major axis of cell morphology perpendicular to stretch insensitive to stretch and promoting maintenance of EC homeostasis.