Mechanotransduction

[1][2][3][4] This form of sensory transduction is responsible for a number of senses and physiological processes in the body, including proprioception, touch,[5] balance, and hearing.

[9] The stimulation of a mechanoreceptor causes mechanically sensitive ion channels to open and produce a transduction current that changes the membrane potential of the cell.

The resultant dynamic modes cannot be generally predicted from static structures of either the entire protein or individual domains.

They can also be suggested by sampling in extensive molecular dynamics trajectories[12] and principal component analysis,[13] or they can be directly observed using spectra[14][15] measured by neutron spin echo spectroscopy.

Due to its unique location at joint surfaces, articular cartilage experiences a range of static and dynamic forces that include shear, compression and tension.

High strain rates (such as which occurs during impact loading) cause tissue damage, degradation, decreased matrix production and apoptosis.

[22][23] Decreased mechanical loading over long periods, such as during extended bed-rest, causes a loss of matrix production.

[citation needed] In addition to binding to ECM ligands, integrins are also receptive to autocrine and paracrine signals such as growth factors in the TGF-beta family.

[35] Recent studies published by Wann et al. in FASEB Journal have demonstrated for the first time that primary cilia are required for chondrocyte mechanotransduction.

Chondrocytes derived from IFT88 mutant mice did not express primary cilia and did not show the characteristic mechanosensitive up regulation of proteoglycan synthesis seen in wild type cells[36] It is important to examine the mechanotransduction pathways in chondrocytes since mechanical loading conditions which represent an excessive or injurious response upregulates synthetic activity and increases catabolic signalling cascades involving mediators such as NO and MMPs.

Thus an improved understanding of the interplay of biomechanics and cell signalling will help to develop therapeutic methods for blocking catabolic components of the mechanotransduction pathway.