Shear stress due to blood flow on endothelial cells elicits numerous responses including G-protein coupled receptor activation and integrin-mediated signaling. Shear-induced change in membrane fluidity has been suggested to be one of the earliest mechanosensing mechanism involved in these processes [1, 2]. Alternatively, it has been suggested that shear forces are transduced through glycocalyx directly to transmembrane proteins and cytoskeleton [3], with very little shear force sensed by the membrane. It is not yet clear whether physiological tensions can alter membrane fluidity significantly.

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