Abstract
Tendon healing is slow and usually results in inferior fibrotic tissue formation. Recently, application of tendon derived stem cells (TDSCs) improved tendon healing in animal studies. In a chicken model, local injection of antioxidants reduced tendon adhesion after tendon injury. An in vitro study demonstrated that supplementation of H2O2 reduced tenogenic marker expression in TDSCs. These findings suggested that the possibility of TDSCs is involved in tendon healing and the cellular activities of TDSCs might be affected by oxidative stress of the local environment. After tendon injury, oxidative stress is increased. Redox modulation might affect healing outcomes via affecting cellular activities in TDSCs. To study the effect of oxidative stress on TDSCs, the cellular activities of rat/human TDSCs were measured under different dosages of vitamin C or H2O2 in this study. Lower dose of vitamin C increased cell proliferation, viability and migration; H2O2 affected colony formation and suppressed cell migration, cell viability, apoptosis, and proliferation. Consistent with previous studies, oxidative stresses (H2O2) affect both recruitment and survival of TDSCs, while the antioxidant vitamin C may exert beneficial effects at low doses. In conclusion, redox modulation affected cellular activities of TDSCs and might be a potential strategy for tendon healing treatment.
Highlights
Tendon injuries, both acute ruptures and chronic degeneration, are a common clinical problem
Tendon progenitor cells (TPC) with pluripotency were identified as one of the cell sources of tendon healing [3, 4] and attempted to use exogenous tendon-derived stem cells (TDSCs) to promote tendon healing are under active investigation [5]
In rat TDSCs, the total number of colonyforming units (CFU) was significantly decreased by incubating with 500 μM vitamin C, and it was mainly due to suppression of CFU-t (p = 0 002), but CFU-f was not affected (p = 0 089)
Summary
Both acute ruptures and chronic degeneration, are a common clinical problem. The process primarily involves activation of progenitor cells and migration of activated cells to the wound, while the amounts of recruited cells would be determined by cell viability, cell proliferation, and programmed cell death. It is well-known that cell recruitment to wound is affected by changes in local biochemical environment after injuries, such as cytokines [2, 6] and oxidative stress [7]. Cell proliferation of TDSCs, as well as the gene expression of tenomodulin and elastin, was significantly suppressed by H2O2 treatment [10].
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