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首页> 外文期刊>Journal of Cellular Physiology >Na(+)/K(+)/Cl(-) cotransporter activates mitogen-activated protein kinase in fibroblasts and lymphocytes.
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Na(+)/K(+)/Cl(-) cotransporter activates mitogen-activated protein kinase in fibroblasts and lymphocytes.

机译：Na (+) / K (+) / Cl(-)转运蛋白激活在成纤维细胞增殖蛋白激酶和淋巴细胞。

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In a previous work, we have shown that overexpression of the Na(+)/K(+)/Cl(-) cotransporter (NKCC1) induces cell proliferation and transformation. We investigate in the present study the role of the NKCC1 in the mitogenic signal transduction. We show that overexpression of the cotransporter gene (NKCC1) in stablely transfected cells (Balb/c-NKCC1), resulted in enhanced phosphorylation of the extracellular regulated kinase (ERK) to produce double phosphorylated ERK (DP-ERK). Furthermore, the level of DP-ERK was reduced by 50-80% following the addition of bumetanide, a specific inhibitor of the Na(+)/K(+)/Cl(-) cotransporter, in quiescent as well as in proliferating cultures of the Balb/c-NKCC1 clone. In order to explore further the role of the Na(+)/K(+)/Cl(-) cotransporter in mitogenic signal transduction, we measured the effect of the two specific inhibitors of the cotransporter; bumetanide and furosemide, on DP-ERK level in immortalized non-transformed cells. In Balb/c 3T3 fibroblasts stimulated with FGF, bumetanide, and furosemide inhibited 50-60% of the ERK 1/2 phosphorylation. The inhibitor concentration needed for maximal inhibition of ERK 1/2 phosphorylation was similar to the concentration needed to block the K(+) influx mediated by the Na(+)/K(+)/Cl(-) cotransporter in these cells. To analyze whether the Na(+)/K(+)/Cl(-) cotransporter has a role in the mitogenic signal of normal cells, we measured the effect of bumetanide on ERK phosphorylation in human peripheral blood lymphocytes. The phosphorylation of ERK 1/2 in resting human lymphocytes, as well as in lymphocytes stimulated with phytohemagglutinin (PHA) was inhibited by bumetanide. The effect of bumetanide on ERK 2 phosphorylation was much lower than that of ERK 1 phosphorylation. The finding that the Na(+)/K(+)/Cl(-) cotransporter controls the ERK/MAPK (mitogen-activated protein kinase) signal transduction pathway, support our hypothesis that Na(+) and K(+) influxes mediated by this transporter plays a central role in the control of normal cell proliferation. Exploring the cellular ionic currents and levels, mediated by the Na(+)/K(+)/Cl(-) cotransporter, should lead to a better comprehension of cell proliferation and transformation machinery.
机译：在以前的工作中,我们已经表明过度的Na (+) / K (+) / Cl (-)转运蛋白(NKCC1)诱导细胞增殖和转换。研究的角色NKCC1促有丝分裂的信号转导。在稳定的转运蛋白基因(NKCC1)转染细胞(Balb / c-NKCC1),导致增强的磷酸化细胞外生产双调节激酶(ERK)磷酸化ERK (DP-ERK)。DP-ERK水平减少50 - 80%以下布美他尼,一个特定的抑制剂Na (+) / K (+) / Cl(-)转运蛋白静以及增殖的文化Balb / c-NKCC1克隆。进一步的角色Na (+) / K (+) / Cl (-)转运蛋白在促有丝分裂的信号转导,我们测量两个特定的效果转运蛋白抑制剂;不灭的呋喃苯胺酸,DP-ERK水平非转换细胞。刺激与FGF、布美他尼和呋喃苯胺酸抑制ERK 1/2磷酸化的50 - 60%。所需的抑制剂浓度最大抑制ERK 1/2磷酸化是相似的所需的浓度来阻止K (+)大量涌入的Na (+) / K (+) / Cl (-)这些细胞的转运蛋白。Na (+) / K (+) / Cl(-)转运蛋白的作用正常细胞的促有丝分裂的信号,我们测量布美他尼ERK的磷酸化的影响人类外周血淋巴细胞。磷酸化ERK 1/2的人休息淋巴细胞,淋巴细胞刺激与植物凝集素(PHA)被抑制布美他尼。ERK的磷酸化是远低于1磷酸化。Na (+) / K (+) / Cl(-)转运蛋白控制ERK / MAPK(增殖蛋白激酶)信号转导通路,支持我们假设Na(+)和K(+)请自来介导通过这个运输中起着重要的作用正常细胞增殖的控制。细胞离子电流和水平,介导Na (+) / K (+) / Cl(-)转运蛋白导致更好的理解细胞扩散和转换机械。

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