Nanette Scutt, Adiv A. Johnson, Andrew Scutt and Alexandra Stolzing
Although ageing predisposes tendons for various pathologies, the effect of ageing on tendon stem/progenitor cells has received little attention. In this study, we compared tendon progenitor cells from patellar, Achilles and tail tendons derived from young (8-12 weeks old) and mature (52 weeks old) rats. The mean number of progenitor cells/ mg was reduced with age in all three tendons and this reduction reached statistical significance in both Achilles and tail tendons. As determined by colony-forming-unit-fibroblasts assays, mean colony number and size were both statistically unchanged with age in patellar and Achilles tendons. In contrast, both colony number and size were significantly reduced in cultures derived from mature tail tendons relative to those derived from young tail tendons. While colonies per mg tissue were reduced with age in all three tendons, this reduction was only statistically significant for tail tendon. Lipofuscin and ROS content in cell progenitors were unchanged with age in all 3 tendons. Conversely, carbonyl content was significantly increased and telomerase activity significantly decreased in mature tail tendon cells relative to young tendon cells. These data suggest that, in the first year of life, rat Achilles and patellar tendons suffer relatively little oxidative damage. In contrast, tail tendons experience an increase protein oxidation, a decrease in telomerase activity and a substantial reduction in progenitor cell numbers. That the source and age of tendon progenitors used influences the quality and density of the progenitor cells isolated from it has important implications for clinical strategies aimed at tendon repair.