Interleukin‑10 promotes proliferation and migration, and inhibits tendon differentiation via the JAK/Stat3 pathway in tendon‑derived stem cells in vitro.
Interleukin‑10 promotes proliferation and migration, and inhibits tendon differentiation via the JAK/Stat3 pathway in tendon‑derived stem cells in vitro.
复制标题
Interleukin10 在体外促进肌腱干细胞的增殖和迁移，并通过 JAK/Stat3 途径抑制肌腱分化。
DOI：
10.3892/mmr.2018.9547
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发表时间：
2018-12
影响因子：
3.4
通讯作者：
Zhang K
中科院分区：
文献类型：
--
作者：
Deng G;Li K;Chen S;Chen P;Zheng H;Yu B;Zhang K
肌腱修复遵循早期炎症、增殖和重塑阶段的缓慢过程，这通常会导致正常生物力学特性的失败和丧失。先前的研究表明，腱源性干细胞（TDSC）是重要的愈合细胞，并且抗炎细胞因子白细胞介素（IL）-10的mRNA表达在炎症后期显着上调。为了探讨 IL-10 如何影响肌腱愈合，本研究研究了 IL-10 对从大鼠跟腱中分离的 TDSC 的体外影响。使用 IL-10 处理后，测量 TDSC 的细胞活性和肌腱细胞标记物的表达水平，并随后进行伤口愈合测定、逆转录定量聚合酶链反应和蛋白质印迹分析。结果表明，IL-10处理显着增加了TDSC的增殖能力。此外，与对照细胞相比，IL-10 显着增强了细胞迁移。此外，IL-10 治疗显着激活 JAK/Stat3 信号通路并抑制肌腱细胞标志物的蛋白表达，包括硬化剂和肌腱调节蛋白。值得注意的是，IL-10 治疗还降低了 TDSC 中 1 型胶原、3 型胶原、lumican 和纤维调节蛋白的基因表达水平。这些发现表明，IL-10 在体外增强 TDSC 的细胞增殖和迁移，并抑制肌腱分化。减少 IL-10 的负面影响，同时增强其正面影响可能是肌腱修复的潜在治疗目标。
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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