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首页> 外文期刊>Brain research >Insulin-like growth factor-I receptor and estrogen receptor crosstalk mediates hormone-induced neurite outgrowth in PC12 cells.
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Insulin-like growth factor-I receptor and estrogen receptor crosstalk mediates hormone-induced neurite outgrowth in PC12 cells.

机译：胰岛素样生长因子-I受体和雌激素受体的串扰介导了PC12细胞中激素诱导的神经突增生。

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摘要

Estradiol (E(2)) and insulin-like growth factor-I (IGF-I) can act independently or in concert to promote neurite outgrowth in vivo and in cultured neurons. This study examined the role of crosstalk between estrogen receptor (ER)alpha and the IGF-I receptor as a critical mediator of hormone- and growth factor-dependent neurite outgrowth in a homogenous cell system. We used control PC12 cells and PC12 cells stably transfected with ER alpha, both of which express IGF-I receptor. Cells were treated for 1 week with vehicle, 1 nM E(2) or 100 ng/ml IGF-I alone or with E(2) or IGF-I in the presence of either the IGF-I receptor antagonist JB1 or the ER antagonist ICI 182,780. IGF-I significantly increased neurite outgrowth, as measured by the percentage of process-bearing cells, and absolute neurite length per cell in both control and ER alpha-transfected PC12 cells. In contrast, E(2) increased process formation and extension only in PC12 cells that were stably transfected with ER alpha. ICI 182,780 and JB1 blocked the IGF-I-induced increases in neurite length in both cell types. The efficacy of ICI 182,780 in control PC12 cells may have been due to the upregulation of ER alpha in these cells by the 7-day treatment with IGF-I. The ER and IGF-I receptor antagonists similarly blocked the E(2)-induced increase in neurite lengths in ER alpha-transfected cells. Immunofluorescent analysis of the cellular distribution of an axonal marker, phospho-neurofilament, verified that the processes extended by PC12 cells were neurites. These data suggest that receptor crosstalk between IGF-I receptors and ER alpha has an important role in neurite formation and extension even in a single-cell system.
机译：雌二醇（E（2））和胰岛素样生长因子-I（IGF-I）可以独立或协同作用，促进体内和培养的神经元中神经突的长出。这项研究检查了雌激素受体（ER）α和IGF-I受体之间的串扰在同质细胞系统中作为激素和生长因子依赖性神经突增生的关键介质的作用。我们使用了稳定的ER12转染的对照PC12细胞和PC12细胞，两者均表达IGF-I受体。在IGF-1受体拮抗剂JB1或ER拮抗剂存在的情况下，分别用溶媒，1 nM E（2）或100 ng / ml IGF-1或E（2）或IGF-1处理细胞1周ICI 182,780。 IGF-1显着增加了神经突向外生长，这是通过带有过程的细胞的百分比以及对照和ERα转染的PC12细胞中每个细胞的绝对神经突长度来衡量的。相反，E（2）仅在被ER alpha稳定转染的PC12细胞中增加了过程形成和扩展。 ICI 182,780和JB1阻止了两种细胞类型中IGF-I诱导的神经突长度的增加。 ICI 182,780在PC12对照细胞中的功效可能是由于用IGF-1处理7天后这些细胞中的ER alpha上调所致。 ER和IGF-I受体拮抗剂类似地阻断ER alpha转染的细胞中E（2）诱导的神经突长度增加。轴突标记物磷酸神经丝的细胞分布的免疫荧光分析证实了PC12细胞延伸的过程是神经突。这些数据表明，即使在单细胞系统中，IGF-I受体与ERα之间的受体串扰在神经突的形成和延伸中也具有重要作用。

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