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首页> 外文期刊>Life sciences >Negative regulation of the protein kinase C activator-induced ICAM-1 expression in the human bronchial epithelial cell line NCI-H292 by p44/42 mitogen-activated protein kinase.
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Negative regulation of the protein kinase C activator-induced ICAM-1 expression in the human bronchial epithelial cell line NCI-H292 by p44/42 mitogen-activated protein kinase.

机译：p44 / 42丝裂原活化蛋白激酶对人支气管上皮细胞株NCI-H292中蛋白激酶C激活剂诱导的ICAM-1表达的负调节。

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摘要

The role of p44/42 mitogen-activated protein kinase (MAPK) in the expression of intercellular adhesion molecule-1 (ICAM-1) in NCI-H292 cells, a human bronchial epithelial cell line, was analyzed. Treatment with the protein kinase C (PKC) activator 12-O-tetradecanoylphorbol 13-acetate (TPA) (16.2 nM) or interferon-gamma (IFN-gamma) (100 U/ml) induced phosphorylation of p44/42 MAPK. The MEK inhibitor U0126 (0.1 to 10 microM) enhanced the TPA-induced ICAM-1 expression but not the IFN-gamma-induced one. U0126 also enhanced the ICAM-1 expression induced by two other PKC activators teleocidin (22.5 nM) and aplysiatoxin (14.9 nM). Furthermore, PD98059 (0.5 to 50 microM), another MEK inhibitor, enhanced the TPA-induced ICAM-1 expression as well. The inhibitor of p38 MAPK SB203580 did not affect the TPA-induced ICAM-1 expression. BAY11-7082, an inhibitor of nuclear factor kappaB (NF-kappaB) activation, and MG132, a 26S proteasome inhibitor, reduced the TPA-induced ICAM-1 expression but not the IFN-gamma-inducedone. TPA partially decreased the level of IkappaB-alpha and the reduction was further augmented by U0126 in a concentration-dependent manner. These findings suggested that, in NCI-H292 cells, p44/42 MAPK suppresses PKC activator-induced NF-kappaB activation, thus negatively regulating the PKC activator-induced ICAM-1 expression but not the IFN-gamma-induced one.
机译：分析了p44 / 42丝裂原活化蛋白激酶（MAPK）在人支气管上皮细胞系NCI-H292细胞中细胞间粘附分子1（ICAM-1）表达中的作用。用蛋白激酶C（PKC）激活剂12-O-十四烷酰佛波醇13-乙酸盐（TPA）（16.2 nM）或干扰素-γ（IFN-γ）（100 U / ml）处理可诱导p44 / 42 MAPK磷酸化。 MEK抑制剂U0126（0.1至10 microM）增强了TPA诱导的ICAM-1表达，但不增强IFN-γ诱导的ICAM-1表达。 U0126还增强了由另外两种PKC激活剂Teleocidin（22.5 nM）和aplysiatoxin（14.9 nM）诱导的ICAM-1表达。此外，另一种MEK抑制剂PD98059（0.5至50 microM）也增强了TPA诱导的ICAM-1表达。 p38 MAPK SB203580的抑制剂不影响TPA诱导的ICAM-1表达。 BAY11-7082，核因子κB（NF-kappaB）激活的抑制剂，和MG132，26S蛋白酶体抑制剂，降低了TPA诱导的ICAM-1表达，但不降低IFN-γ诱导的酮。 TPA部分降低了IkappaB-alpha的水平，U0126以浓度依赖性的方式进一步降低了IkappaB-alpha的水平。这些发现表明，在NCI-H292细胞中，p44 / 42 MAPK抑制PKC激活剂诱导的NF-kappaB的激活，从而负调控PKC激活剂诱导的ICAM-1的表达，而不是IFN-γ诱导的表达。

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