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Oxydative stress alters nuclear shape through lamins dysregulation

机译：氧化胁迫通过层叠液改变核形状

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摘要

Progeroid phenotypes are mainly encountered in 2 types of syndromes: in laminopathies, which are characterized by nuclear shape abnormalities due to lamin A alteration, and in DNA damage response defect syndromes. Because lamin A dysregulation leads to DNA damages, it has been proposed that senescence occurs in both types of syndromes through the accumulation of damages. We recently showed that elevated oxidative stress is responsible for lamin B1 accumulation, nuclear shape alteration and senescence in the DDR syndrome, ataxia telangiectasia (A-T). Interestingly, overexpression of lamin B1 in wild type cells is sufficient to induce senescence without the induction of DNA damages. Here, we will discuss the importance of controlling the lamins level in order for maintenance nuclear architecture and we will comment the relationships of lamins with other senescence mechanisms. Finally, we will describe emerging data reporting redox control by lamins, leading us to propose a general mechanism by which reactive oxygen species can induce senescence through lamin dysregulation and NSA.
机译：Progeroid表型主要遇到2种类型的综合征：在层板疗法中，其特征在于核形状异常，由于层压发生变化，并且在DNA损伤反应缺陷综合征中。因为Lamin a失呼量导致DNA损坏，所以已经提出了通过损坏的积累来衰老发生在两种类型的综合症中。我们最近表明，氧化应激升高负责DDR综合征，Ataxia Telanciectasia（A-T）中的Lamin B1积累，核形状改变和衰老。有趣的是，在野生型细胞中的Lamin B1的过度表达足以诱导衰老而不诱导DNA损伤。在这里，我们将讨论控制Lamins级别以进行维护核建筑的重要性，我们将评论Lamins与其他衰老机制的关系。最后，我们将描述Lamins的新兴数据报告氧化还原控制，导致我们提出一种通过Lamin Dysregulation和NSA可以诱导衰老的一般机制。

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