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Mechanical force modulates scleraxis expression in bioartificial tendons

Scott, A (författare)
University of British Columbia, and Centre for Hip Health and Mobility, Vancouver Coastal Health Research Institute, Vancouver
Danielson, Patrik (författare)
Umeå universitet,Anatomi
Abraham, T (författare)
James Hogg Research Centre-St Paul’s Hospital, Vancouver;
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Fong, G (författare)
University of British Columbia, and Centre for Hip Health and Mobility, Vancouver Coastal Health Research Institute, Vancouver
Sampaio, A V (författare)
University of British Columbia
Underhill, T M (författare)
University of British Columbia
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 (creator_code:org_t)
International Society of Musculoskeletal and Neuronal Interactions, 2011
Engelska.
Ingår i: Journal of Musculoskeletal and Neuronal Interactions - JMNI. - : International Society of Musculoskeletal and Neuronal Interactions. - 1108-7161. ; 11:2, s. 124-132
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
Stäng  
  • Following tendon injury, cartilage, bone and fat metaplasia are often observed, making the optimization of tenocyte differentiation an important clinical goal. In this study we examined the effect of static and cyclic mechanical loading on the expression of genes which play a role in tenocyte differentiation and function, namely scleraxis (Scx) and Type I collagen (Col1a1), and determined the effect of varying mechanical parameters including (1) static vs dynamic load, (2) increasing strain magnitude, (3) inclusion of 10 s rest periods, and (4) increasing cycle number. Cyclic loading resulted in a greater increase of tenocyte gene expression than static loading over 3 weeks in culture. Increasing strain levels potentiated the induction of tenocyte genes. The insertion of a 10 s rest periods further enhanced tenocyte gene expression, as did increasing repetition numbers. These results suggest that mechanical signaling exerts an important influence on the expression of genes which play a role in determining the tendon phenotype. Further work is required to confirm and extend these findings in primary cells such as resident tendon progenitor/stem cells, in order to provide an improved understanding of biology from which optimized rehabilitation programs can be developed.

Nyckelord

Tenocyte
Mechanotransduction
Tendinopathy

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