IL-17A promotes the growth of airway epithelial cells through ERK-dependent signaling pathway

被引：51

作者：

Inoue, Daisuke

Numasaki, Muneo

Watanabe, Mika

Kubo, Hiroshi

Sasaki, Takahiko

Yasuda, Hiroyasu

Yamaya, Mutsuo

Sasaki, Hidetada

机构：

[1] Tohoku Univ, Dept Geriatr & Resp Med, Sch Med, Aoba Ku, Sendai, Miyagi 9808574, Japan

[2] Tohoku Univ Hosp, Dept Pathol, Aoba Ku, Sendai, Miyagi 9808574, Japan

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2006年 / 347卷 / 04期

关键词：

IL-17A; mucin; airway epithelial cells; and mitogen-activated protein kinase kinase;

D O I：

10.1016/j.bbrc.2006.06.137

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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.

引用

页码：852 / 858

页数：7

共 36 条

[1]

Antonysamy M.A., 2003, CYTOKINE HDB

[2] IL-13-induced changes in the goblet cell density of human bronchial epithelial cell cultures: MAP kinase and phosphatidylinositol 3-kinase regulation [J].