Role of p38MAPK and oxidative stress in copper-induced senescence
Role of p38MAPK and oxidative stress in copper-induced senescence
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DOI：
10.1007/s11357-013-9521-3
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发表时间：
2013-12-01
期刊：
影响因子：
--
通讯作者：
Toussaint, Olivier
中科院分区：
文献类型：
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作者：
Boilan, Emmanuelle;Winant, Virginie;Toussaint, Olivier
在目前的工作中，我们表明，铜是参与人二倍体成纤维细胞的衰老，我们描述的机制来解释it.Using不同的技术，我们首次显示在细胞复制衰老过程中铜的积累。这种积聚似乎与脂褐素共定位。其次，我们观察到，与硫酸铜孵育的细胞诱导氧化应激，抗氧化反应和过早衰老。抗氧化分子减少了过早衰老的出现。第三，我们发现Nrf2转录因子被激活并调节参与抗氧化反应的基因的表达，而p38（MAPK）调节早衰的出现。
In the present work, we indicate that copper is involved in the senescence of human diploid fibroblasts and we describe mechanisms to explain it. Using different techniques, we show for the first time an accumulation of copper in cells during replicative senescence. This accumulation seems to be co-localized with lipofuscin. Second, we observed that an incubation of cells with copper sulfate induced oxidative stress, antioxidant response and premature senescence. Antioxidant molecules reduced the appearance of premature senescence. Third, we found that Nrf2 transcription factor was activated and regulated the expression of genes involved in antioxidant response while p38(MAPK) regulated the appearance of premature senescence.