Abstract
It is known that mechanical loading of muscles increases the strength of healing tendon tissue, but the mechanism involved remains elusive. We hypothesized that the secretome from myoblasts in co-culture with tenocytes affects tenocyte migration, cell phenotype, and collagen (Col) production and that the effect is dependent on different types of mechanical loading of myoblasts. To test this, we used an in vitro indirect transwell co-culture system. Myoblasts were mechanically loaded using the FlexCell® Tension system. Tenocyte cell migration, proliferation, apoptosis, collagen production, and several tenocyte markers were measured. The secretome from myoblasts decreased the Col I/III ratio and increased the expression of tenocyte specific markers as compared with tenocytes cultured alone. The secretome from statically loaded myoblasts significantly enhanced tenocyte migration and Col I/III ratio as compared with dynamic loading and controls. In addition, the secretome from statically loaded myoblasts induced tenocytes towards a myofibroblast-like phenotype. Taken together, these results demonstrate that the secretome from statically loaded myoblasts has a profound influence on tenocytes, affecting parameters that are related to the tendon healing process.
Highlights
IntroductionIt is thought that the effect of loading during tendon healing is exerted through mechanotransduction, i.e., that cells detect mechanical loading and transform this into a cellular response [5,6,7,8]
Mechanical loading is well known to improve tendon healing [1,2,3,4]
We first examined the effect of myoblast secretome on tenocytemigration migrationininco-culco-culture ture with mechanically unloaded myoblasts using a transwell assay
Summary
It is thought that the effect of loading during tendon healing is exerted through mechanotransduction, i.e., that cells detect mechanical loading and transform this into a cellular response [5,6,7,8]. Another theory is that mechanical loading might induce microdamage of healing tissue which triggers inflammation [9]. Both of these theories focus on local events within the tendon. While muscle–bone crosstalk has been extensively studied (reviewed by [11,12,13]), muscle–tendon crosstalk has so far been largely disregarded
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