Repair of cyclobutane pyrimidine dimers or dimethylsulfate damage in DNA is identical in normal or telomerase-immortalized human skin fibroblasts.
Repair of cyclobutane pyrimidine dimers or dimethylsulfate damage in DNA is identical in normal or telomerase-immortalized human skin fibroblasts.
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DOI：
10.1093/nar/gki542
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发表时间：
2005
影响因子：
14.9
通讯作者：
O'Connor, TR
中科院分区：
文献类型：
--
作者：
Bates, SE;Zhou, NY;Federico, LE;Xia, L;O'Connor, TR
正常细胞在体内和体外衰老的过程伴随着端粒长度的减少，端粒是每个连锁群末端的染色体帽片段。然而，核糖核蛋白端粒酶的逆转录酶亚基（HTERT）的过表达恢复端粒长度并延迟细胞衰老。虽然在文献中存在一些关于存活的数据，但没有分子数据表明端粒酶永生化细胞中的DNA修复是正常的。从原代人成纤维细胞系构建了几种端粒酶永生化的人皮肤成纤维细胞系。用紫外线（UV）辐射或硫酸二甲酯（DMS）处理原代细胞系和端粒酶永生化细胞系。UV辐射主要产生通过核苷酸切除修复修复的环丁烷嘧啶二聚体，而DMS主要引入通过碱基切除修复修复的N-甲基嘌呤。在这里，我们表明，在端粒酶永生化的人皮肤成纤维细胞系的两种类型的损伤的修复是相同的，在正常皮肤成纤维细胞中观察到的修复。因此，端粒酶表达和皮肤成纤维细胞的永生化不会改变人类细胞中的核苷酸或碱基切除修复。
The progression of a normal cell to senescence in vivo and in vitro is accompanied by a reduction in the length of the telomeres, the chromosome capping segments at the end of each linkage group. However, overexpression of the reverse transcriptase subunit (HTERT) of the ribonucleoprotein telomerase restores telomere length and delays cellular senescence. Although some data exist in the literature with respect to survival, no molecular data have shown that DNA repair in telomerase-immortalized cells is normal. Several telomerase-immortalized human skin fibroblast cell lines were constructed from a primary human fibroblast cell line. The primary line and the telomerase-immortalized cell lines were treated with either ultraviolet (UV) radiation or dimethylsulfate (DMS). UV radiation principally produces cyclobutane pyrimidine dimers that are repaired by nucleotide excision repair, whereas DMS introduces mainly N-methylpurines repaired by base excision repair. Here, we show that repair of both types of damage in the telomerase-immortalized human skin fibroblast cell lines is identical to repair observed in normal skin fibroblasts. Thus, telomerase expression and consequent immortalization of skin fibroblasts do not alter nucleotide or base excision repair in human cells.
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影响因子：
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