Permanent embryo arrest: molecular and cellular concepts.
Permanent embryo arrest: molecular and cellular concepts.
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DOI：
10.1093/molehr/gan035
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发表时间：
2008-08
影响因子：
4
通讯作者：
Madan P
中科院分区：
文献类型：
--
作者：
Betts DH;Madan P
发育停滞是导致体外发育第一周胚胎死亡水平升高的机制之一。大约10-15%的IVF胚胎在2- 4细胞分裂阶段永久性地停止有丝分裂，没有细胞凋亡的迹象。活性氧（ROS）参与了这一过程，必须加以控制，以优化胚胎生产。p66 Shc是一种对氧化应激进行免疫应答的衔接蛋白，它是一种应激传感器，可以为永久性细胞周期停滞提供关键的理解，并将ROS与细胞信号传导途径联系起来。小鼠中p66 Shc基因的缺失导致寿命延长，这与它们对氧化应激的抵抗力增强和细胞凋亡水平降低有关。p66 Shc已被证明可以产生线粒体H2 O2来触发细胞凋亡，但也可能作为许多影响线粒体功能的信号通路的整合点。我们已经检测到在停滞的胚胎中p66 Shc和ROS水平升高，并认为p66 Shc在调节永久性胚胎停滞中起着核心作用。在本文中，我们回顾了永久胚胎停滞的细胞和分子方面，并推测这种胚胎死亡方法的机制和病因。
Developmental arrest is one of the mechanisms responsible for the elevated levels of embryo demise during the first week of in vitro development. Approximately 10–15% of IVF embryos permanently arrest in mitosis at the 2- to 4-cell cleavage stage showing no indication of apoptosis. Reactive oxygen species (ROS) are implicated in this process and must be controlled in order to optimize embryo production. A stress sensor that can provide a key understanding of permanent cell cycle arrest and link ROS with cellular signaling pathway(s) is p66Shc, an adaptor protein for apoptotic-response to oxidative stress. Deletion of the p66Shc gene in mice results in extended lifespan, which is linked to their enhanced resistance to oxidative stress and reduced levels of apoptosis. p66Shc has been shown to generate mitochondrial H2O2 to trigger apoptosis, but may also serve as an integration point for many signaling pathways that affect mitochondrial function. We have detected elevated levels of p66Shc and ROS within arrested embryos and believe that p66Shc plays a central role in regulating permanent embryo arrest. In this paper, we review the cellular and molecular aspects of permanent embryo arrest and speculate on the mechanism(s) and etiology of this method of embryo demise.
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