We chose a model of skeletal tissue regeneration because of the well documented mechanosensitive properties of the skeleton [45], and in so doing, gained critical insights into how skeletal progenitor cells sense a mechanical force, interpret these forces, and then respond by altering their behavior.
As a quantum mechanical force field, these energy terms are approximated by empirical functions in the spirit of conventional molecular mechanics.
The association of integrins with cytoskeletal proteins is crucial for the transmission of biochemical signals and mechanical force across these adhesion receptors and, thus, for integrin-mediated cell functions, such as spreading, migration, and gene expression.
As the mechanical force generated by these muscles is easily measurable, the pathology of these muscles might be identified by assessment of the isometric strengths of these muscles with comparison with the data in normal population.
However, calcium ion entry through the plasma membrane due to a mechanical force does not require these contractile proteins only the cytoskeleton is involved.
Interestingly, polycystin 1-knockout mice exhibited a reduced ability to respond with increased bone formation to an external mechanical force, and osteoblasts from these mice did have a reduced ability to respond to fluid flow in vitro with an intracellular Ca2+ signal (47).
Applying subtle mechanical forces to these systems, they may be also deformed into non-spherical shapes.
Also quite different is the sensitivity for the measurement of mechanical forces of these two hardware systems.
They provide an integrin-based system for the transduction of mechanical forces between these cells and the surrounding ECM [ 72, 81].
The authors suggested that differences in mechanical forces in these regions may explain the regulation when obtaining tendon-proper tissue regeneration or chondrogenic tissue degeneration.
