Interleukin-10 promotes proliferation and migration, and inhibits tendon differentiation via the JAK/Stat3 pathway in tendon-derived stem cells in vitro

Tendon repair follows a slow course of early inflammatory, proliferative and remodeling phases, which commonly results in the failure and loss of normal biomechanical properties. Previous studies have demonstrated that tendon-derived stem cells (TDSCs) are vital healing cells and that mRNA expression of anti-inflammatory cytokine interleukin (IL)-10 is significantly upregulated at the late inflammatory phase. To explore how IL-10 may impact tendon healing, the present study investigated the in vitro effects of IL-10 on TDSCs isolated from rat Achilles tendons. Cellular activities of TDSCs and the expression levels of tendon cell markers were measured treatment with IL-10 and subsequent performance of wound healing assays, reverse transcription-quantitative polymerase chain reaction and western blot analyses. The results demonstrated that IL-10 treatment markedly increased the proliferative capacity of TDSCs. In addition, IL-10 significantly enhanced cell migration when compared with the control cells. Furthermore, IL-10 treatment significantly activated the JAK/Stat3 signaling pathway and inhibited the protein expression of tendon cell markers, including scleraxis and tenomodulin. Notably, IL-10 treatment also reduced the gene expression levels of type 1 collagen, type 3 collagen, lumican and fibromodulin in TDSCs. These findings indicated that IL-10 enhanced cell proliferation and migration, and inhibited tenogenic differentiation in TDSCs in vitro. Reducing the negative effects whilst enhancing the positive effects of IL-10 may be a potential therapeutic target in tendon repair.