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首页> 外文期刊>The journals of gerontology.Series A. Biological sciences and medical sciences >Effects of telomerase and viral oncogene expression on the in vitro growth of human chondrocytes.
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Effects of telomerase and viral oncogene expression on the in vitro growth of human chondrocytes.

机译：端粒酶和病毒致癌基因表达对人软骨细胞体外生长的影响。

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Senescent chondrocytes accumulate with aging in articular cartilage, a process that interferes with cartilage homeostasis and increases the risk of cartilage degeneration. We showed previously that chondrocyte telomere length declines with donor age, which suggests that the aging process is telomere dependent. From these results we hypothesized that telomerase should delay the onset of senescence in cultured chondrocytes. Population doubling limits (PDL) were determined for chondrocytes expressing telomerase. We found that telomerase alone did not extend PDL beyond controls that senesced after 25 population doublings. The human papillomavirus 16 oncogenes E6 and E7 were transduced into the same cell population to investigate this telomere-independent form of senescence further. Chondrocytes expressing E6 and E7 grew longer than the telomerase cDNA (hTERT) cells but still senesced at 55 population doublings. In contrast, chondrocytes expressing telomerase with E6 and E7 grew vigorously past 100 population doublings. We conclude that although telomerase is necessary for the indefinite extension of chondrocyte life span, telomere-independent senescence limits PDL in vitro and may play a role in the age-related accumulation of senescent chondrocytes in vivo.
机译：衰老的软骨细胞随着关节软骨的衰老而积累，这一过程会干扰软骨的稳态并增加软骨变性的风险。先前我们表明，软骨细胞端粒的长度随供体年龄而下降，这表明衰老过程是端粒依赖性的。根据这些结果，我们推测端粒酶应延迟培养的软骨细胞衰老的开始。确定了表达端粒酶的软骨细胞的群体倍增极限（PDL）。我们发现，端粒酶本身并不能将PDL扩展到25倍人口增加后引起衰老的对照。人类乳头瘤病毒16个癌基因E6和E7被转导到相同的细胞群中，以进一步研究这种端粒非依赖性形式的衰老。表达E6和E7的软骨细胞比端粒酶cDNA（hTERT）细胞长，但仍能在55个种群倍增时衰老。相比之下，表达端粒酶的E6和E7软骨细胞在100倍人口增长中急剧生长。我们得出结论，尽管端粒酶对于无限期延长软骨细胞的寿命是必需的，但端粒独立的衰老限制了体外的PDL并可能在体内衰老的软骨细胞的年龄相关积累中发挥作用。

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