Our study characterizes how physical signals, determine the nucleoskeletal architecture of the stem cell repository of bone forming cells. As alterations in nuclear-cytoplasmic components have been strongly linked to cellular senescence, the loss of differentiation potential during aging might be due to dysfunction of this particular aspect of cell structure. Our proposed studies also have the potential to identify the LINC complex as a regulatory element that prevents MSC responsiveness and subsequent musculoskeletal repair via limiting the accessible spectrum of mechanical information to which MSC can respond. Findings from these studies will carry the field forward by identifying and mechanically characterizing force-induced adaptations of the subcellular architecture.
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