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Biochem Biophys Res Commun. 2017 Mar 4;484(2):422-428. doi: 10.1016/j.bbrc.2017.01.142. Epub 2017 Jan 28.

Amphiregulin suppresses epithelial cell apoptosis in lipopolysaccharide-induced lung injury in mice.

Author information

1
Research Institute for Diseases of the Chest, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
2
Research Institute for Diseases of the Chest, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. Electronic address: yanagiha@kokyu.med.kyushu-u.ac.jp.
3
Division of Respiratory Diseases, Department of Internal Medicine, Jikei University School of Medicine, Tokyo, Japan.

Abstract

BACKGROUND AND OBJECTIVE:

As a member of the epidermal growth factor family, amphiregulin contributes to the regulation of cell proliferation. Amphiregulin was reported to be upregulated in damaged lung tissues in patients with chronic obstructive pulmonary disease and asthma and in lung epithelial cells in a ventilator-associated lung injury model. In this study, we investigated the effect of amphiregulin on lipopolysaccharide (LPS)-induced acute lung injury in mice.

METHODS:

Acute lung injury was induced by intranasal instillation of LPS in female C57BL/6 mice, and the mice were given intraperitoneal injections of recombinant amphiregulin or phosphate-buffered saline 6 and 0.5 h before and 3 h after LPS instillation. The effect of amphiregulin on apoptosis and apoptotic pathways in a murine lung alveolar type II epithelial cell line (LA-4 cells) were examined using flow cytometry and western blotting, respectively.

RESULTS:

Recombinant amphiregulin suppressed epithelial cell apoptosis in LPS-induced lung injury in mice. Western blotting revealed that amphiregulin suppressed epithelial cell apoptosis by inhibiting caspase-8 activity.

CONCLUSION:

Amphiregulin signaling may be a therapeutic target for LPS-induced lung injury treatment through its prevention of epithelial cell apoptosis.

KEYWORDS:

Amphiregulin; Apoptosis; Lipopolysaccharide

PMID:
28137591
DOI:
10.1016/j.bbrc.2017.01.142
[Indexed for MEDLINE]
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