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首页> 外文期刊>Cell biology international. >ERK signaling pathway is differentially involved in erythroid differentiation of K562 cells depending on time and the inducing agent.
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ERK signaling pathway is differentially involved in erythroid differentiation of K562 cells depending on time and the inducing agent.

机译：根据时间和诱导剂的不同，ERK信号通路与K562细胞的红系分化有关。

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摘要

K562 cells can be induced to differentiate along the erythroid lineage by a variety of chemical compounds, including hemin, butyrate, cisplatin and ara-C. Differential signaling through MAP kinases has been suggested to be involved in this differentiation process. We have investigated the involvement of ERK activation/inhibition in hemin-, butyrate-, cisplatin- and ara-C-induced erythroid differentiation using the K562 cell line. ERK activity decreased for 2-4h after administration of either inducing agent. ERK was then activated by hemin and cisplatin, while ERK phosphorylation remained decreased during incubation with butyrate and ara-C. There was no activation of JNK or p38. The MEK-1 inhibitors UO126 or PD98059 induced erythroid differentiation in K562 cells and acted additively with butyrate. Inhibition of MEK-1 reduced the hemoglobin accumulation by hemin and cisplatin; erythroid differentiation by ara-C was unchanged. The results suggest that inhibition of signaling through ERK in K562 cells maybe needed to enter the erythroid differentiation process, while after initiation both activation and inhibition of signaling through ERK enhance erythroid differentiation, which, however, is dependent on the inducing compound.
机译：可以通过多种化合物（包括血红素，丁酸，顺铂和ara-C）诱导K562细胞沿红系谱系分化。已经建议通过MAP激酶的差异信号转导参与该分化过程。我们已经研究了使用K562细胞系ERK激活/抑制在血红素，丁酸，顺铂和ara C诱导的类红细胞分化中的作用。任一种诱导剂给药后2-4小时，ERK活性下降。然后用血红素和顺铂激活ERK，而在与丁酸酯和ara-C孵育期间ERK的磷酸化作用仍然降低。没有激活JNK或p38。 MEK-1抑制剂UO126或PD98059诱导K562细胞中的类红细胞分化，并与丁酸盐相加。抑制MEK-1可减少血红素和顺铂对血红蛋白的积累; ara-C对红系的分化没有改变。结果表明，可能需要在K562细胞中通过ERK抑制信号进入红系分化过程，而在启动后，激活和通过ERK抑制信号均会增强红系分化，但是这取决于诱导化合物。

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