Role of p38MAPK and oxidative stress in copper-induced senescence

被引：33

作者：

Boilan, Emmanuelle ^{[1
]}

Winant, Virginie ^{[1
]}

Dumortier, Elise ^{[1
]}

Piret, Jean-Pascal ^{[1
]}

Bonfitto, Francois ^{[1
]}

Osiewacz, Heinz D. ^{[2
]}

Debacq-Chainiaux, Florence ^{[1
]}

Toussaint, Olivier ^{[1
]}

机构：

[1] Univ Namur FUNDP, NARILIS URBC, B-5000 Namur, Belgium

[2] Goethe Univ Frankfurt, Inst Mol Biosci, D-60054 Frankfurt, Germany

来源：

AGE | 2013年 / 35卷 / 06期

关键词：

Aging; Senescence; Copper; Metals; p38(MAPK); Oxidative stress; Human fibroblasts; FUNGUS PODOSPORA-ANSERINA; LIFE-SPAN CONTROL; PREMATURE SENESCENCE; HUMAN FIBROBLASTS; CELLULAR SENESCENCE; MITOCHONDRIAL-DNA; IN-VITRO; CELLS; TOXICITY; DISEASE;

D O I：

10.1007/s11357-013-9521-3

中图分类号：

R592 [老年病学]; C [社会科学总论];

学科分类号：

03 ; 0303 ; 100203 ;

摘要：

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.

引用

页码：2255 / 2271

页数：17

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