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首页> 外文期刊>Aging cell. >Telomere uncapping during in vitro T-lymphocyte senescence.
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Telomere uncapping during in vitro T-lymphocyte senescence.

机译：在体外T淋巴细胞衰老过程中端粒解开。

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摘要

Normal lymphocytes represent examples of somatic cells that are able to induce telomerase activity when stimulated. As previously reported, we showed that, during lymphocyte long-term culture and repeated stimulations, the appearance of senescent cells is associated with telomere shortening and a progressive drop in telomerase activity. We further showed that this shortening preferentially occured at long telomeres and was interrupted at each stimulation by a transitory increase in telomere length. In agreement with the fact that telomere uncapping triggers lymphocyte senescence, we observed an increase in gamma-H2AX and 53BP1 foci as well as in the percentage of cells exhibiting DNA damage foci in telomeres. Such a DNA damage response may be related to the continuous increase of p16(ink4a) upon cell stimulation and cell aging. Remarkably, at each stimulation, the expression of shelterin genes, such as hTRF1, hTANK1, hTIN2, hPOT1 and hRAP1, was decreased. We propose that telomere dysfunction during lymphocyte senescence caused by iterative stimulations does not only result from an excessive telomere shortening, but also from a decrease in shelterin content. These observations may be relevant for T-cell biology and aging.
机译：正常淋巴细胞代表体细胞的例子，当受到刺激时它们能够诱导端粒酶活性。如先前报道，我们表明，在淋巴细胞长期培养和反复刺激过程中，衰老细胞的出现与端粒缩短和端粒酶活性的逐步下降有关。我们进一步表明，这种缩短优先发生在长端粒上，并在每次刺激时被端粒长度的短暂增加所中断。与端粒解封会触发淋巴细胞衰老的事实相一致，我们观察到了γ-H2AX和53BP1病灶以及端粒中表现出DNA损伤病灶的细胞百分比的增加。这种DNA损伤反应可能与细胞刺激和细胞衰老后p16（ink4a）的持续增加有关。显着地，在每次刺激下，庇护素基因如hTRF1，hTANK1，hTIN2，hPOT1和hRAP1的表达降低。我们提出，由反复刺激引起的淋巴细胞衰老过程中的端粒功能异常不仅是端粒缩短过多，而且是由于棚菌素含量降低所致。这些观察结果可能与T细胞生物学和衰老有关。

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