Abstract
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.
Highlights
The normal ageing process gives rise to a series of degenerative changes in connective and musculoskeletal tissues
Tissues were excised and weighed, progenitor cells extracted by collagenase digestion, cell number determined and the number of progenitor cells per mg tissue calculated for each tendon group (Table 1)
Like we found with autofluorescence, there was no significant difference between mature and young progenitor cells derived from patellar, Achilles and tail tendons (Figure 5b)
Summary
The normal ageing process gives rise to a series of degenerative changes in connective and musculoskeletal tissues. These changes lead to increased frailty, a decline in functional competence and a reduction in the ability to cope with bodily stresses [1,2]. As connective tissue healing generally becomes impaired with age [10,11], it is likely that poor tendon healing is exacerbated in the elderly. This has been shown to be the case in a rat model of rotator cuff repair, where aging diminished tendon-to-bone healing [12]
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