Gene-specific DNA repair of pyrimidine dimers does not decline during cellular aging in vitro
Gene-specific DNA repair of pyrimidine dimers does not decline during cellular aging in vitro
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DOI：
10.1006/excr.2000.4826
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发表时间：
2000-04-10
影响因子：
3.7
通讯作者：
Rattan, SIS
中科院分区：
文献类型：
--
作者：
Christiansen, M;Stevnsner, T;Rattan, SIS
大量研究表明，衰老过程中各种DNA损伤不断累积，而DNA修复能力下降可能是其原因之一。然而，总基因组修复水平与衰老并没有很强的相关性。众所周知，某些损伤的 DNA 修复与转录过程密切相关。因此，我们选择使用人二倍体皮肤成纤维细胞和小梁成骨细胞的体外衰老作为衰老模型系统来研究紫外线引起的损伤的基因特异性修复水平。我们发现，在人皮肤成纤维细胞和小梁成骨细胞培养物的细胞老化过程中，总基因组修复并未受到显着影响。对细胞衰老过程中二氢叶酸还原酶管家基因、p53 肿瘤抑制基因和失活区域 X-754 的基因特异性修复进行了分析。在任何分析的基因中，年轻和年老细胞修复紫外线诱导的嘧啶二聚体的能力没有明显差异。因此，体外衰老细胞可以维持修复外部诱导损伤的能力。 (C) 2000 年学术出版社。
A large number of studies have demonstrated that various kinds of DNA damage accumulate during aging and one of the causes for this could be a decrease in DNA repair capacity. However, the level of total genomic repair has not been strongly correlated with aging. DNA repair of certain kinds of damage is known to be closely connected to the transcription process; thus, we chose to investigate the level of gene-specific repair of UV-induced damage using in vitro aging of human diploid skin fibroblasts and trabecular osteoblasts as model systems for aging. We find that the total genomic repair is not significantly affected during cellular aging of cultures of both human skin fibroblasts and trabecular osteoblasts. Gene-specific repair was analyzed during cellular aging in the dihydrofolate reductase housekeeping gene, the p53 tumor suppressor gene, and the inactive region X-754. There was no clear difference in the capacity of young and old cells to repair UV-induced pyrimidine dimers in any of the analyzed genes. Thus, in vitro senescent cells can sustain the ability to repair externally induced damage. (C) 2000 Academic Press.