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首页> 外文期刊>Cytokine >The mitogen-activated protein kinase p38 is necesssary for interleukin 1beta-induced monocyte chemoattractant protein 1 expression by human mesangial cells.
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The mitogen-activated protein kinase p38 is necesssary for interleukin 1beta-induced monocyte chemoattractant protein 1 expression by human mesangial cells.

机译：有丝分裂原激活的蛋白激酶p38是人肾小球系膜细胞表达白介素1β诱导的单核细胞趋化蛋白1所必需的。

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Mitogen-activated protein (MAP) kinases have been suggested as potential mediators for interleukin 1beta (IL-1beta)-induced gene activation. This study investigated the role of the MAP kinases p38 and ERK2 in IL-1beta-mediated expression of the chemokine MCP-1 by human mesangial cells. Phosphorylation of p38 kinase, which is necessary for activation, increased significantly after IL-1beta treatment. p38 kinase immunoprecipitated from IL-1beta-treated cells phosphorylated target substrates to a greater extent than p38 kinase from controls. SB 203580, a selective p38 kinase inhibitor, was used to examine the role of p38 kinase in MCP-1 expression. SB 203580 decreased IL-1beta-induced MCP-1 mRNA and protein levels, but did not affect MCP-1 mRNA stability. Because NF-kappaB is necessary for MCP-1 gene expression, the effect of p38 kinase inhibition on IL-1beta induction of NF-kappaB was measured. SB 203580 (up to 25 microM) had no effect on IL-1beta-induced NF-kappaB nuclear translocation or DNA binding activity. Our previous work showed that IL-1beta also activates the MAP kinase ERK2 in human mesangial cells. PD 098059, a selective inhibitor of the ERK activating kinase MEK1, had no effect on IL-1beta-induced MCP-1 mRNA or protein levels, or on IL-1beta activation of NF-kappaB. These data indicate that p38 kinase is necessary for the induction of MCP-1 expression by IL-1beta, but is not involved at the level of cytoplasmic activation of NF-kappaB. In contrast, ERK2 does not mediate IL-1beta induced MCP-1 gene expression. Copyright 1999 Academic Press.
机译：丝裂原激活的蛋白（MAP）激酶已被建议作为白介素1beta（IL-1beta）诱导的基因激活的潜在介质。这项研究调查了MAP激酶p38和ERK2在人肾小球系膜细胞IL-1beta介导的趋化因子MCP-1表达中的作用。 IL-1β处理后，激活所必需的p38激酶的磷酸化显着增加。从IL-1β处理的细胞中免疫沉淀的p38激酶比靶标的p38激酶在更大程度上磷酸化了靶底物。 SB 203580是一种选择性p38激酶抑制剂，用于检查p38激酶在MCP-1表达中的作用。 SB 203580降低了IL-1β诱导的MCP-1 mRNA和蛋白质水平，但不影响MCP-1 mRNA的稳定性。由于NF-κB对于MCP-1基因表达是必需的，因此测量了p38激酶抑制对NF-κBIL-1β诱导的影响。 SB 203580（最大25 microM）对IL-1β诱导的NF-κB核移位或DNA结合活性没有影响。我们以前的工作表明，IL-1beta还可以激活人系膜细胞中的MAP激酶ERK2。 PD 098059是ERK活化激酶MEK1的选择性抑制剂，对IL-1beta诱导的MCP-1 mRNA或蛋白质水平或NF-kappaB的IL-1beta活化均无影响。这些数据表明，p38激酶对于通过IL-1beta诱导MCP-1表达是必需的，但在NF-κB的细胞质活化水平上并不参与。相反，ERK2不介导IL-1beta诱导的MCP-1基因表达。版权所有1999，学术出版社。

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