Cutaneous wound healing is a complex process that aims to re-establish the original structure of the skin and its functions. Among other disorders, peripheral neuropathies are known to severely impair wound healing capabilities of the skin, revealing the importance of skin innervation for proper repair. Here, we report that peripheral glia are crucially involved in this process. Using a mouse model of wound healing, combined with in vivo fate mapping, we show that injury activates peripheral glia by promoting de-differentiation, cell-cycle re-entry and dissemination of the cells into the wound bed. Moreover, injury-activated glia upregulate the expression of many secreted factors previously associated with wound healing and promote myofibroblast differentiation by paracrine modulation of TGF-β signalling. Accordingly, depletion of these cells impairs epithelial proliferation and wound closure through contraction, while their expansion promotes myofibroblast formation. Thus, injury-activated glia and/or their secretome might have therapeutic potential in human wound healing disorders.

中文翻译：

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损伤激活的神经胶质细胞促进小鼠成年皮肤的伤口愈合。

皮肤伤口愈合是一个复杂的过程，旨在重建皮肤的原始结构及其功能。在其他疾病中，已知周围神经病会严重损害皮肤的伤口愈合能力，从而揭示皮肤神经支配对适当修复的重要性。在这里，我们报告说周围神经胶质细胞参与了这一过程。使用伤口愈合的小鼠模型，结合体内命运图谱，我们显示出损伤通过促进去分化，细胞周期再进入和细胞向伤口床的扩散而激活周围神经胶质细胞。此外，损伤激活的神经胶质通过旁分泌调节TGF-β信号传导，上调了许多以前与伤口愈合有关的分泌因子的表达，并促进了成纤维细胞的分化。因此，这些细胞的消耗会损害上皮的增殖和通过收缩引起的伤口闭合，而它们的扩增则促进成肌纤维细胞的形成。因此，损伤激活的神经胶质和/或它们的分泌组可能在人类伤口愈合疾病中具有治疗潜力。