衰老
细胞凋亡
程序性细胞死亡
DNA断裂
碎片(计算)
细胞生物学
成纤维细胞
过氧化氢
细胞培养
DNA损伤
细胞
细胞生长
体外
老化
化学
生物
分子生物学
DNA
生物化学
遗传学
生态学
作者
Eui‐Ju Yeo,Yong-Chul Hwang,Chang‐Mo Kang,Hyon E. Choy,Sang Chul Park
出处
期刊:Molecules and Cells
[Korean Society for Molecular and Cellular Biology]
日期:2000-08-01
卷期号:10 (4): 415-422
被引量:57
标识
DOI:10.1016/s1016-8478(23)17496-6
摘要
We studied mechanisms by which senescent cells acquire resistance to UV-induced cellular insults. Human primary foreskin fibroblast culture was used since it undergoes cellular senescence in vitro after a limited number of passages. Senescence was induced by a brief treatment of the early passage cells with 100 μM of H2O2 for 1 h, and subsequent culture for 3 weeks. Hydrogen peroxide-treated cells showed an enhancement of senescence-associated β-galactosidase activity. In the senescent cells, DNA fragmentation in response to UV-irradiation was found to decrease significantly compared with that in the young cells. The SAPK/JNK activation by UV irradiation was reduced in both non-treated senescent cells and the hydrogen peroxide-induced senescent cells, suggesting that a reduced DNA fragmentation by UV-irradiation in the senescent cells is closely related to the decreased SAPK/JNK activity. Since a cell cycle inhibitor, p21Waf1, has been implicated in protecting cells against apoptotic cell death, we determined p21Waf1 to assess whether its elevation has any impact on the reduction of UV-induced activation of SAPK/JNK in the senescent cells. The expression of p21Waf1 increased in both the non-treated and the hydrogen peroxide-treated senescent cells. Our study also revealed that the blockage of SAPK/JNK activation in the senescent cells was closely related to the increased level of p21Waf1. Our observation might provide clues about molecular mechanism of resistance to DNA fragmentation and the consequent cell death by UV-irradiation.
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