Arterial endothelial cells are subjected to cyclic stretch during the cardiac cycle, which affects intracellular signaling and gene expression to regulate cellular functions such as apoptosis, proliferation and morphology. Actin stress fibers (SFs) within adherent nonmuscle cells generate isometric tension to counterbalance forces in the extracellular matrix and maintain mechanical equilibrium. This equilibrium is disrupted by external mechanical cues and SFs can either relax or reorient themselves in an effort to reestablish equilibrium (Hsu et al. 2009). However, the mechanism by which cells determine their specific response to particular changes in mechanical stretch remains unclear.

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