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首页> 外文会议>3rd International EMF Seminar in China: Electromagnetic Fields and Biological Effects; Oct 13-17, 2003; Guilin, China >THE EFFECT OF PULSED ELECTRIC FIELD ON THE LEVEL OF TYROSINE PHOSPHORYLATION AND GENE EXPRESSION LEVEL OF HUMAN HEPATOCYTES MEDIATED BY INSULIN
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THE EFFECT OF PULSED ELECTRIC FIELD ON THE LEVEL OF TYROSINE PHOSPHORYLATION AND GENE EXPRESSION LEVEL OF HUMAN HEPATOCYTES MEDIATED BY INSULIN

机译：脉冲电场对胰岛素介导人肝细胞酪氨酸磷酸化水平和基因表达水平的影响

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Protein-tyrosine phosphatases (PTPases) play an essential role in the regulation of reversible tyrosine phosphorylation of cellular proteins that mediate insulin action. In the gene expression experiment, we found that an increase in tyrosine phosphatase expression level of 2.4-fold. Li PM concluded that overexpression of the protein-tyrosine phosphatase LAR in hepatoma cells suppressed the insulin receptor activation. Kulas DT discovered that overexpression of the transmembrane protein-tyrosine phosphatase (PTPase) CD45 in nonhematopoietic cell results in decreased signaling through growth factor receptor tyrosine kinases. The increased PTPases level might be responsible for the cell proliferation inhibition caused by the exposed insulin. But the tyrosine kinase expression level also increased 2.8 fold, which added to the complexity of the possible cell proliferation reason. Hirsch's experiments indicated that the inhibitors of tyrosine kinases and tyrosine phosphatases could be the promoter mitogenic activation. The long-term treatment of exposed insulin might downregulate some unknown inhibitors that promoted proliferation, thus both the tyrosine kinase and phosphatase was raised. Another possible reason was that the expression level of the tyrosine kinase, tyrosine phophatase and the small GTP-bind protein were raised in order to make up for the partially imcompetence of the exposed insulin molecule to activate the cell growth. The signal pathway could be affected by the exposed insulin, which means that the exposure signal could be transferred into the cells and influence their metabolism and proliferation indirectly. Our studies shed light on the fact that the EM field changed the structure of the insulin molecule. The molecule carried the exposure signal into the cell, affected the level of tyrosine phosphorylation and the gene expression level by the decrease of binding capability with the insulin receptor and consequently inhibited cell proliferation, (see Fig 1).These studies proposed that: the intercellular signal molecule such as insulin can be the target of the electromagnetic field and acts as a signal carrying the imformation of PEF, which consequently causes biological effects.
机译：蛋白质酪氨酸磷酸酶（PTPases）在调节介导胰岛素作用的细胞蛋白质的可逆酪氨酸磷酸化中起重要作用。在基因表达实验中，我们发现酪氨酸磷酸酶表达水平增加了2.4倍。 Li PM得出结论，肝癌细胞中蛋白酪氨酸磷酸酶LAR的过表达抑制了胰岛素受体的激活。 Kulas DT发现，非造血细胞中跨膜蛋白酪氨酸磷酸酶（PTPase）CD45的过表达导致通过生长因子受体酪氨酸激酶的信号减少。 PTPases水平升高可能是由暴露的胰岛素引起的细胞增殖抑制所致。但是酪氨酸激酶的表达水平也增加了2.8倍，这增加了可能的细胞增殖原因的复杂性。 Hirsch的实验表明，酪氨酸激酶和酪氨酸磷酸酶的抑制剂可能是启动子的促有丝分裂活化。暴露的胰岛素的长期治疗可能下调一些未知的促进增殖的抑制剂，因此酪氨酸激酶和磷酸酶均升高。另一个可能的原因是，酪氨酸激酶，酪氨酸磷酸酶和小的GTP结合蛋白的表达水平升高，以弥补暴露的胰岛素分子的部分功能丧失，从而激活细胞生长。信号途径可能受到暴露的胰岛素的影响，这意味着暴露的信号可以转移到细胞中并间接影响其代谢和增殖。我们的研究揭示了电磁场改变了胰岛素分子结构的事实。该分子将暴露信号传递到细胞中，通过降低与胰岛素受体的结合能力，从而影响酪氨酸磷酸化水平和基因表达水平，从而抑制细胞增殖（见图1）。这些研究提出：诸如胰岛素之类的信号分子可能是电磁场的目标，并充当携带PEF信息的信号，从而引起生物学效应。

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