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首页> 美国卫生研究院文献>The Journal of Clinical Investigation >Relationship between proliferation and cell cycle-dependent Ca2+ influx induced by a combination of thyrotropin and insulin-like growth factor-I in rat thyroid cells.
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Relationship between proliferation and cell cycle-dependent Ca2+ influx induced by a combination of thyrotropin and insulin-like growth factor-I in rat thyroid cells.

机译：甲状腺素和胰岛素样生长因子-I联合诱导大鼠甲状腺细胞增殖与细胞周期依赖性Ca2 +流入之间的关系。

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The mechanism of cell proliferation by a combination of thyroid-stimulating hormone (TSH) and insulin-like growth factor-I (IGF-I) was studied in rat thyroid (FRTL-5) cells. IGF-I stimulated an approximately 3.5-fold increase in the rate of Ca2+ influx sustained for at least 6 h in TSH-pretreated cells but not in quiescent cells. The significant cell proliferation was observed when TSH-primed cells were incubated with IGF-I for 24 h but not for 12 h. IGF-I stimulated the rate of Ca2+ influx in a dose-dependent manner that was similar to that for induction of DNA synthesis. Both Ca2+ influx and DNA synthesis observed in response to IGF-I in TSH-primed cells were inhibited by cobalt. In addition, the stimulations of Ca2+ influx and DNA synthesis by IGF-I were dependent on extracellular Ca2+ in TSH-pretreated cells. When TSH-primed cells were pretreated with pertussis toxin, both IGF-I-induced Ca2+ influx and DNA synthesis were abolished. However, pertussis toxin did not block the priming action of TSH or forskolin. When calcium entry was induced by Bay K8644, it stimulated cell growth in TSH-primed cells but not in quiescent cells. Moreover, cobalt and lanthanum inhibited DNA synthesis even when added several hours after the addition of Bay K8644 but not when added 24 h after the growth factor in TSH-primed cells. These findings suggest that at least two important mechanisms may work in response to IGF-I only in the TSH-primed G1 phase of the cell cycle: first, IGF-I can activate directly or indirectly the Ca2+ channel via a pertussis toxin-sensitive substrate in TSH-primed cells; and second, a long lasting calcium entry by IGF-I may be a cell cycle-dependent mitogenic signal.
机译：在大鼠甲状腺（FRTL-5）细胞中研究了甲状腺刺激激素（TSH）和胰岛素样生长因子-I（IGF-1）结合产生的细胞增殖机制。在TSH预处理的细胞中，IGF-I刺激持续至少6小时的Ca2 +流入速率增加了约3.5倍，而在静止细胞中则没有。当TSH引发的细胞与IGF-I孵育24小时而不是12小时时，观察到了显着的细胞增殖。 IGF-I以剂量依赖性方式刺激Ca 2+流入的速率，其方式类似于诱导DNA合成。在TSH启动的细胞中，观察到的对IGF-I的反应中Ca2 +内流和DNA合成均受到钴的抑制。另外，IGF-I对Ca 2+内流和DNA合成的刺激取决于TSH预处理细胞中的细胞外Ca 2+。当用百日咳毒素预处理TSH致敏细胞时，IGF-I诱导的Ca2 +内流和DNA合成均被取消。但是，百日咳毒素并未阻止TSH或毛喉素的启动作用。当Bay K8644诱导钙进入时，它刺激了TSH启动的细胞中的细胞生长，但不刺激静止细胞中的细胞生长。此外，即使在添加Bay K8644数小时后添加，钴和镧也能抑制DNA合成，而在TSH诱导的细胞中，在生长因子后24小时添加时，钴和镧也不能抑制DNA合成。这些发现表明，至少有两个重要的机制可能仅在细胞周期的TSH诱导的G1期响应IGF-I：首先，IGF-I可以通过百日咳毒素敏感底物直接或间接激活Ca2 +通道。在TSH致敏细胞中；其次，IGF-I持久的钙进入可能是细胞周期依赖性有丝分裂信号。

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