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首页> 外文期刊>Journal of Biomechanics >Tendon healing in interleukin-4 and interleukin-6 knockout mice.
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Tendon healing in interleukin-4 and interleukin-6 knockout mice.

机译：白介素4和白介素6基因敲除小鼠的肌腱愈合。

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Cytokines have been shown to play an important role in tendon and ligament healing by regulating cellular differentiation and activity. The majority of studies that have investigated the role of cytokines in tendon and ligament healing have added them to injured tissue and assessed their effect. Because the efficacy of exogenously applying cytokines is dependent upon many factors such as the correct dosage, timing, and frequency, conflicting results are often reported. To avoid these factors, this study used transgenic mice with knockouts of interleukin-4 (IL4 -/-) and interleukin-6 (IL6 -/-) to investigate their role in tendon healing. Because of the reported roles of both of these cytokines in inflammation and fibroplasia, it was hypothesized that the order of organizational, geometric, and mechanical properties would be (greatest to least) injured IL6 -/-, injured control, and injured IL4 -/- mice. In addition, it was hypothesized that specific cytokines would be upregulated in each knockout group, but not compensate for the lack of IL-4 or IL-6. Mechanical and organizational properties of injured tendons from IL6 -/- mice were inferior to that of control and IL4 -/- mice despite the upregulation of the pro-inflammatory cytokine TNF-alpha. Temporal levels of IL-10 and IL-13 in the IL4 -/- mice resulted in comparable and even superior properties when compared to CTL mice. This study shows that IL-6 could not be compensated for and plays an important role in tendon healing. This study also supports the use of this animal model to further investigate tendon healing.
机译：已经证明细胞因子通过调节细胞分化和活性在肌腱和韧带愈合中起重要作用。研究细胞因子在肌腱和韧带愈合中作用的大多数研究已将它们添加到受伤的组织中并评估了它们的作用。由于外源性应用细胞因子的功效取决于许多因素，例如正确的剂量，时间和频率，因此经常会报告相互矛盾的结果。为了避免这些因素，本研究使用了具有白介素4（IL4-/-）和白介素6（IL6-/-）剔除的转基因小鼠，研究它们在肌腱愈合中的作用。由于据报道这两种细胞因子均在炎症和纤维化中发挥作用，因此假设组织，几何和机械特性的顺序为（最大至最小）IL6-/-损伤，对照损伤和IL4-/损伤- 老鼠。另外，假设在每个基因敲除组中特定的细胞因子将被上调，但不能弥补IL-4或IL-6的缺乏。尽管促炎性细胞因子TNF-α上调，但来自IL6-/-小鼠的受伤肌腱的机械和组织特性不如对照组和IL4-/-小鼠。与CTL小鼠相比，IL4-/-小鼠中IL-10和IL-13的时间水平导致了相当甚至更好的特性。这项研究表明IL-6不能得到补偿，并且在肌腱愈合中起重要作用。这项研究还支持使用该动物模型进一步研究腱的愈合。

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