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首页> 外文会议>International EMF seminar in China: Electromagnetic fields and biological effects >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的人肝细胞酪氨酸磷酸化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（PTP酶）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的增加为2.4倍。李PM得出结论，肝脏瘤细胞中蛋白质 - 酪氨酸磷酸酶LAR的过度表达抑制了胰岛素受体活化。 Kulas DT发现，跨膜蛋白 - 酪氨酸磷酸酶（PTP酶）CD45在非发育细胞中的过度表达导致通过生长因子受体酪氨酸激酶的信号传导降低。增加的ptpases水平可能负责由暴露的胰岛素引起的细胞增殖抑制。但酪氨酸激酶表达水平也增加了2.8倍，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以是启动子促毒性活化。暴露胰岛素的长期治疗可能下调一些促进增殖的未知抑制剂，因此培养酪氨酸激酶和磷酸酶。另一种可能的原因是培养酪氨酸激酶，酪氨酸激酶，酪氨酸磷酸酶和小GTP结合蛋白的表达水平，以便构成暴露的胰岛素分子的部分嵌入以激活细胞生长。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EM场改变了胰岛素分子结构的事实。该分子将曝光信号纳入细胞，影响酪氨酸磷酸化水平和基因表达水平通过与胰岛素受体的结合能力降低，并因此抑制细胞增殖，（参见图1）。这些研究提出：细胞诸如胰岛素的信号分子可以是电磁场的靶，并且作为携带PEF的变形的信号作用，从而导致生物效应。

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