Sustained production of ROS triggers compensatory proliferation and is required for regeneration to proceed.

Sustained production of ROS triggers compensatory proliferation and is required for regeneration to proceed.
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DOI:
10.1038/srep02084
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发表时间:
2013
期刊:
影响因子:
4.6
通讯作者:
Vriz, Sophie
Vriz, Sophie
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Gauron, Carole;Rampon, Christine;Bouzaffour, Mohamed;Ipendey, Eliane;Teillon, Jeremie;Volovitch, Michel;Vriz, Sophie

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再生医学中的一个主要问题是损伤在促进细胞可塑性中的作用。在这里,我们探讨活性氧(ROS)诱导成年斑马鱼病变的功能。我们发现,ROS的产生,成年鳍截肢后,在时间和空间上受到严格的调节,至少24小时,而ROS的产生仍然是短暂的(2小时),在单纯的伤口愈合。在再生组织中,ROS信号传导触发两个不同的平行途径:一个途径负责细胞凋亡,另一个途径负责JNK激活。这两个事件都参与了残端表皮细胞的代偿性增殖,并且是再生进展所必需的。这两种事件都影响Wnt、SDF 1和IGF途径,而细胞凋亡仅影响祖细胞标志物表达。这些结果暗示了再生中的氧化应激,并为愈合和再生之间的差异提供了新的见解。
A major issue in regenerative medicine is the role of injury in promoting cell plasticity. Here we explore the function of reactive oxygen species (ROS) induced through lesions in adult zebrafish. We show that ROS production, following adult fin amputation, is tightly regulated in time and space for at least 24 hours, whereas ROS production remains transient (2 hours) in mere wound healing. In regenerative tissue, ROS signaling triggers two distinct parallel pathways: one pathway is responsible for apoptosis, and the other pathway is responsible for JNK activation. Both events are involved in the compensatory proliferation of stump epidermal cells and are necessary for the progression of regeneration. Both events impact the Wnt, SDF1 and IGF pathways, while apoptosis only impacts progenitor marker expression. These results implicate oxidative stress in regeneration and provide new insights into the differences between healing and regeneration.
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