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Signalling cascades in mechanotransduction: cell-matrix interactions and mechanical loading

Ramage, L.; Nuki, G.; Salter, D. M.

Authors

L. Ramage

G. Nuki

D. M. Salter



Abstract

Mechanical loading of articular cartilage stimulates the metabolism of resident chondrocytes and induces the synthesis of molecules to maintain the integrity of the cartilage. Mechanical signals modulate biochemical activity and changes in cell behavior through mechanotransduction. Compression of cartilage results in complex changes within the tissue including matrix and cell deformation, hydrostatic and osmotic pressure, fluid flow, altered matrix water content, ion concentration and fixed charge density. These changes are detected by mechanoreceptors on the cell surface, which include mechanosensitive ion channels and integrins that on activation initiate intracellular signalling cascades leading to tissue remodelling. Excessive mechanical loading also influences chondrocyte metabolism but unlike physiological stimulation leads to a quantitative imbalance between anabolic and catabolic activity resulting in depletion of matrix components. In this article we focus on the role of mechanical signalling in the maintenance of articular cartilage, and discuss how alterations in normal signalling can lead to pathology.

Citation

Ramage, L., Nuki, G., & Salter, D. M. (2009). Signalling cascades in mechanotransduction: cell-matrix interactions and mechanical loading. Scandinavian Journal of Medicine and Science in Sports, 19(4), 457-469. https://doi.org/10.1111/j.1600-0838.2009.00912.x

Journal Article Type Article
Acceptance Date Dec 19, 2008
Online Publication Date Jun 15, 2009
Publication Date 2009-08
Deposit Date Mar 25, 2017
Journal Scandinavian Journal of Medicine & Science in Sports
Print ISSN 0905-7188
Electronic ISSN 1600-0838
Publisher Wiley
Peer Reviewed Peer Reviewed
Volume 19
Issue 4
Pages 457-469
DOI https://doi.org/10.1111/j.1600-0838.2009.00912.x
Keywords mechanotransduction, cartilage, chondrocyte,
Public URL http://researchrepository.napier.ac.uk/Output/819821




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