IL-17A promotes the growth of airway epithelial cells through ERK-dependent signaling pathway
IL-17A promotes the growth of airway epithelial cells through ERK-dependent signaling pathway
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DOI：
10.1016/j.bbrc.2006.06.137
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发表时间：
2006-09-08
影响因子：
3.1
通讯作者：
Sasaki, Hidetada
中科院分区：
文献类型：
--
作者：
Inoue, Daisuke;Numasaki, Muneo;Sasaki, Hidetada
观察IL-17A对气道上皮细胞粘蛋白生成和生长的影响。组织学和免疫组织化学分析显示，IL-17A增加了气液界面培养中气管上皮细胞的粘蛋白产量和数量。采用ELISA法测定IL-17A刺激气管上皮细胞产生粘蛋白的生物学特性。Calcein-AM法证实IL-17A对气管上皮细胞有丝分裂作用。IL-17A的生长刺激作用是剂量依赖性的，并通过ERK MAP激酶途径介导。MEK抑制剂可以消除IL-17A的有丝分裂作用，而p38或JNK抑制剂则没有明显的抑制作用。此外，相对较低剂量的IL-13也通过与IL-17A不同的信号通路显著促进气管上皮细胞的生长。这些发现提供了IL-17A通过ERK MAP激酶途径刺激气道上皮细胞生长的第一个证据。(c) 2006爱思唯尔公司版权所有。
The effects of IL-17A on mucin production and growth of airway epithelial cells were examined. Histological and immunohistochemical analyses revealed that IL-17A increased the mucin production and number of tracheal epithelial cells in air-liquid interface cultures. The biological property of IL-17A to stimulate the mucin production by tracheal epithelial cells was determined using an ELISA. The mitogenic effect of IL-17A on tracheal epithelial cells was confirmed with Calcein-AM assay. The growth-stimulatory effect of IL-17A was dose-dependent and mediated via the ERK MAP kinase pathway. Inhibitors of MEK abrogated the mitogenic effect of IL-17A, whereas an inhibitor of p38 or JNK displayed no significant inhibitory effect. Moreover, relatively lower doses of IL-13 also significantly increased the growth of tracheal epithelial cells through a distinct signaling pathway from that of IL-17A. These findings provide the first evidence that IL-17A stimulates the growth of airway epithelial cells through the ERK MAP kinase pathway. (c) 2006 Elsevier Inc. All rights reserved.