I read in {1}:

The matrix is far more conspicuous than the cells. However, it is now widely recognised that the cellular elements hold the key to understanding development, repair and the ability of tendons and ligaments to respond to changing mechanical load. Tenocytes are mechanosensitive cells that are hardwired in a way that allows them to deploy a tensegrity architectural system to detect changes in mechanical load via deformation of their cell membrane and cytoskeleton (Wang, 2006). Strain in the extracellular matrix (ECM) tenses cytoskeletal fibres via integrin receptors in the cell membrane, and this in turn is relayed to the cell nucleus so that gene expression can be altered. An important principle of the tensegrity system is fibre continuity between the ECM and the cells. As Myers et al. (2007) point out, the implication is that the existence of a continuous network of fibres (i.e. collagen fibres in the ECM; cytoskeletal fibres in the cells) means that stress on one part of one cell can be dissipated throughout the entire tissue. Consequently, individual cells are protected from damage and a small mechanical stimulus can potentially affect many cells (Ingber, 1997; Myers et al., 2007). It is also worth noting that an under-stimulation of tenocytes that results from an altered cell–ECM interaction consequent upon tendinopathy could down-regulate cell activity (Arnoczky et al., 2007). Thus, the tendon becomes weakened and more vulnerable to damage from mechanical overload.

For how long is the gene expression altered in tenocytes' nuclei following changes in mechanical load, and which genes are affected?



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