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

白细胞介素-10 促进体外肌腱干细胞增殖和迁移,并通过 JAK/Stat3 通路抑制肌腱分化

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作者:Ganming Deng, Kaiqun Li, Siwei Chen, Peisheng Chen, Haonan Zheng, Bin Yu, Kairui Zhang

Abstract

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.

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