Abstract
BackgroundHealing of tendons after injury involves the proliferation of tenocytes and the production of extracellular matrix; however, their capacity to heal is limited by poor cell density and limited growth factor activity. Flightless I (Flii) has previously been identified as an important regulator of cellular proliferation and migration, and the purpose of this study was to evaluate the effect of differential Flii gene expression on tenocyte function in vitro.MethodsThe role of Flii on tenocyte proliferation, migration, and contraction was assessed using established assays. Tenocytes from Flii+/−, wild-type, and Flii overexpressing mice were obtained and the effect of differential Flii expression on migration, proliferation, contraction, and collagen synthesis determined in vitro. Statistical differences were determined using unpaired Student’s t test and statistical outliers were identified using the Grubbs’ test.ResultsFlii overexpressing tenocytes showed significantly improved migration and proliferation as well as increased collagen I secretion. Explanted tendons from Flii overexpressing mice also showed significantly elevated tenocyte outgrowth compared to Flii+/− mice. In contrast to its role in dermal wound repair, Flii positively affects cellular processes in tendons.ConclusionsThese findings suggest that Flii could be a novel target for modulating tenocyte activity and improving tendon repair. This could have significant clinical implications as novel therapeutic targets for improved healing of tendon injuries are urgently needed.
Highlights
Healing of tendons after injury involves the proliferation of tenocytes and the production of extracellular matrix; their capacity to heal is limited by poor cell density and limited growth factor activity
Tenocytes express Tenascin-C and Scleraxis Digital tendons were removed from Flightless I (Flii)+/−, WT, and FliiTg/Tg mice, the tendon sheath was removed by microscopic dissection, and intrinsic tenocytes were isolated by outgrowth or enzyme digestion methods (Fig. 1)
Tenascin-C and Scleraxis were expressed in Flii+/−, WT, and FliiTg/Tg tenocytes with no expression seen in fibroblasts from the same mice, (Fig. 1b–g)
Summary
Healing of tendons after injury involves the proliferation of tenocytes and the production of extracellular matrix; their capacity to heal is limited by poor cell density and limited growth factor activity. Tendons inherently have minimal capacity for healing owing to poor cell density and growth factor activity [1]. Tenocytes have long cellular processes which facilitate cell-extracellular matrix (ECM) and cell-cell communication through desmosomes and tight junctions [2]. They are highly metabolically active and are responsible for synthesizing and secreting ECM. Proliferation, and contraction are essential processes that allow tendon healing to occur.
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
