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标题:增殖的神经干细胞内源高ROS水平通过PI3K/AKT依赖性的信号通路调节其自我更新和神经发生
6 [4 `- u n _2 W6 } U3 m2 ]; l" |原文标题:Proliferative Neural Stem Cells Have High Endogenous ROS Levels that Regulate Self-Renewal and Neurogenesis in a PI3K/Akt-Dependant Manner
/ G$ z. l0 J3 g" Z# i/ T摘要翻译: 绝大多数的ROS研究都集中阐述ROS的细胞毒性. 干细胞可以通过相关的机理来维持自身较低水平的ROS,进而减少ROS带来的细胞毒性.但是,最近的一些研究表明ROS可以作为第二信使, 活化正常的细胞过程.在这篇文章中,作者们研究了ROS在分离的大脑神经祖细胞 (progenitors)中功能.有点很意外的是, 具有神经干细胞的特点的增殖的多能神经祖细胞有很高的ROS水平,而且对ROS增高有很强的反应性.ROS介导的多能祖细胞的增殖和神经生成是依赖于PI3K/AKt信号通路. 体外和体内的实验表明,通过药物或者遗传学的方法来降低/消除细胞内ROS的水平影响到正常神经干细胞和/或者祖细胞的功能.这篇文章揭示了,氧化还原介导的机制在神经干细胞功能维持中的作用,并且这个机制在脑损伤,疾病和修复中有很重要的指导意义.# H' i; Y, H) O9 |
原文摘要:The majority of research on reactive oxygen species (ROS) has focused on their cellular toxicities. Stem cells generally have been thought to maintain low levels of ROS as a protection against these processes. However, recent studies suggest that ROS can also play roles as second messengers, activating normal cellular processes. Here, we investigated ROS function in primary brain-derived neural progenitors. Somewhat surprisingly, we found that proliferative, self-renewing multipotent neural progenitors with the phenotypic characteristics of neural stem cells (NSC) maintained a high ROS status and were highly responsive to ROS stimulation. ROS-mediated enhancements in self-renewal and neurogenesis were dependent on PI3K/Akt signaling. Pharmacological or genetic manipulations that diminished cellular ROS levels also interfered with normal NSC and/or multipotent progenitor function both in vitro and in vivo. This study has identified a redox-mediated regulatory mechanism of NSC function that may have significant implications for brain injury, disease, and repair." B* H& h" @( D' g# D1 i
原文链接:http://www.cell.com/cell-stem-ce ... 5909%2810%2900650-8: p% M; U" P( X6 R
Note: 个人翻译,理解不准确的语句还望大家积极指出.
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