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

Daisuke Inoue; Muneo Numasaki; Mika Watanabe; Hiroshi Kubo; Takahiko Sasaki; Hiroyasu Yasuda; Mutsuo Yamaya; Hidetada Sasaki

doi:10.1016/j.bbrc.2006.06.137

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

Daisuke Inoue, Muneo Numasaki, Mika Watanabe, Hiroshi Kubo, Takahiko Sasaki, Hiroyasu Yasuda, Mutsuo Yamaya, Hidetada Sasaki

Research output: Contribution to journal › Article › peer-review

47 Citations (Scopus)

Abstract

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.

Original language	English
Pages (from-to)	852-858
Number of pages	7
Journal	Biochemical and biophysical research communications
Volume	347
Issue number	4
DOIs	https://doi.org/10.1016/j.bbrc.2006.06.137
Publication status	Published - 2006 Sep 8

Keywords

Airway epithelial cells, and mitogen-activated protein kinase kinase
IL-17A
Mucin

ASJC Scopus subject areas

Biophysics
Biochemistry
Molecular Biology
Cell Biology

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IL-17A promotes the growth of airway epithelial cells through ERK-dependent signaling pathway. / Inoue, Daisuke; Numasaki, Muneo ; Watanabe, Mika; Kubo, Hiroshi; Sasaki, Takahiko; Yasuda, Hiroyasu; Yamaya, Mutsuo; Sasaki, Hidetada.

In: Biochemical and biophysical research communications, Vol. 347, No. 4, 08.09.2006, p. 852-858.

Research output: Contribution to journal › Article › peer-review

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abstract = "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.",

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AU - Inoue, Daisuke

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AU - Watanabe, Mika

AU - Kubo, Hiroshi

AU - Sasaki, Takahiko

AU - Yasuda, Hiroyasu

AU - Yamaya, Mutsuo

AU - Sasaki, Hidetada

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N2 - 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.

AB - 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.

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KW - Mucin

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

Abstract

Keywords

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