Genetic effects on the longevity of cultured human fibroblasts. II. DNA repair deficient syndromes.
Genetic effects on the longevity of cultured human fibroblasts. II. DNA repair deficient syndromes.
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遗传对培养的人类成纤维细胞寿命的影响。
DOI：
10.1159/000213097
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发表时间：
1983
期刊：
影响因子：
3.5
通讯作者：
R. Holliday
中科院分区：
文献类型：
--
作者：
K. Thompson;R. Holliday
已经测量了来自具有降低的DNA修复或染色体稳定性的遗传综合征的成纤维细胞的寿命。与对照组相比，来自Bloom综合征、Cockayne综合征、Fanconi贫血和共济失调毛细血管扩张症3例中的2例的细胞具有显著降低的生长潜力。在每种情况下，测量了几个平行群体的寿命，并观察到Cockayne综合征细胞的寿命变化最大。来自1名共济失调毛细血管扩张症患者和1名弗里德赖希共济失调患者的成纤维细胞生长至对照培养物中观察到的传代水平。结果表明，修复过程是细胞实现其最大体外寿命所必需的，并支持错误理论而不是衰老的程序理论。
The lifespan of fibroblasts from genetic syndromes with reduced DNA repair or chromosome stability has been measured. Cells from Bloom's syndrome, Cockayne's syndrome, Fanconi's anaemia and 2 out of 3 cases of ataxia telangiectasia had a significantly reduced growth potential in comparison to controls. In each case the longevity of several parallel populations was measured and the greatest variability in lifespan was observed with Cockayne's syndrome cells. The fibroblasts from 1 ataxia telangiectasia patient and a Friedreich's ataxia patient grew to the passage levels seen in control cultures. The results suggest that repair processes are necessary for cells to achieve their maximum in vitro lifespan, and support the error theory rather than the programme theory of ageing.