ABSTRACT
It is now well recognized that tissue cells have the ability to sense their extracellular environment and respond by adapting their structure, internal tension, and mechanical properties [22], modulating their function without being subjected to external forces [13,48]. From soft to stiff substrates, it has been shown that: (1) cell spreading is increased and stress fibers are reinforced in epithelial cells, fibroblasts, and smooth muscle cells but not always in neutrophils [26]; and (2) cell migration is facilitated due to larger intracellular traction forces and cell spreading area is increased [34]. Moreover, the function of certain cells has been found optimal in an intermediate range of environmental stiffness. This is the case with skeletal muscle cells, which optimally differentiate when they grow on substrates with stiffness close to muscle tissue stiffness [15]. It should be emphasized that tissues have very different stiffness levels; a normal tissue might have very different elastic properties. With a Young’s modulus on the order of 0.5 kPa, brain appears the softest tissue. Muscles have a Young’s modulus of 10 kPa. The Young’s modulus of skin is approximately 102 kPa while that of bones reaches up to 106kPa. Most importantly, pathophysiological phenomena develop in the context of altered extracellular
mechanical properties. The role of these properties on the disease processes is not fully understood. This is the case for tumor progression, which is modulated by substrate and extracellular matrix (ECM) mechanical properties [49]. The definition of new therapeutic processes such as nerve tissue engineering, encapsulated cell therapies and self-renewal and differentiation of stem cells also requires considering biophysical cues in addition to biochemical cues. It has been shown that the rate of neurite extension and branching critically depends on substrate rigidity [32]. Moreover, the mechanical properties of the stem cell’s microenvironment regulate its behavior [41].
