Amputation-induced reactive oxygen species are required for successful Xenopus tadpole tail regeneration.
Amputation-induced reactive oxygen species are required for successful Xenopus tadpole tail regeneration.
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DOI：
10.1038/ncb2659
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发表时间：
2013-02
影响因子：
21.3
通讯作者：
中科院分区：
文献类型：
--
作者：
了解促进成功组织再生的分子机制对于再生医学的持续发展至关重要。非洲爪蟾（Xenopus laevis）和热带爪蟾（Xenopus tropicalis）物种的脊椎两栖类蝌蚪具有在截肢后通过多种生长因子信号传导途径（包括Wnt、Fgf、BMP、notch和TGFβ途径）的协调活性再生其尾巴的显著能力。然而，我们对损伤后这些信号通路上游的活动知之甚少。在这里，我们表明，非洲爪蟾蝌蚪尾部截肢诱导持续生产的活性氧（ROS）在尾部再生。通过药理学或遗传学方法降低ROS水平会减少细胞增殖并损害尾部再生。基因拯救实验恢复了ROS的产生和再生反应的启动。持续增加的ROS水平是Wnt/β-连环蛋白信号传导和其主要下游靶标之一fgf 20的激活所必需的，而fgf 20又是适当的尾部再生所必需的。这些发现表明损伤诱导的ROS产生是组织再生的重要调节因子。
Understanding the molecular mechanisms that promote successful tissue regeneration is critical for continued advancements in regenerative medicine. Vertebrate amphibian tadpoles of the species Xenopus laevis and Xenopus tropicalis have remarkable abilities to regenerate their tails following amputation , via the coordinated activity of numerous growth factor signaling pathways, including the Wnt, Fgf, BMP, notch, and TGFβ pathways . Little is known, however, about the events that act upstream of these signalling pathways following injury. Here, we show that Xenopus tadpole tail amputation induces a sustained production of reactive oxygen species (ROS) during tail regeneration. Lowering ROS levels, via pharmacological or genetic approaches, reduces cell proliferation and impairs tail regeneration. Genetic rescue experiments restored both ROS production and the initiation of the regenerative response. Sustained increased ROS levels are required for Wnt/β-catenin signaling and the activation of one of its major downstream targets, fgf20 , which, in turn, is essential for proper tail regeneration. These findings demonstrate that injury-induced ROS production is an important regulator of tissue regeneration.
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