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Involvement of retinoic acid-inducible gene-I in the IFN-/STAT1 signalling pathway in BEAS-2B cells

¹ Depts of Vascular Biology, Institute of Brain Science, and ² Internal Medicine, Hirosaki University School of Medicine, Hirosaki, and ³ Dept of Tumour Biology, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan

CORRESPONDENCE: T. Imaizumi, Dept of Vascular Biology, Institute of Brain Science, Hirosaki University School of Medicine, 5-Zaifu-cho, Hirosaki 036-8562, Japan. Fax: 81 172395135. E-mail: timaizum@cc.hirosaki-u.ac.jp

Keywords: BEAS-2B, interferon-, interferon--inducible protein 10, retinoic acid-inducible gene-I, signal transducer and activator of transcription 1

Received: September 1, 2004
Accepted February 9, 2005

Bronchial epithelial cells play an important role in airway host defence, and interferon (IFN)- controls immune reactions by regulating the expression of various genes in bronchial epithelial cells. Signal transducer and activator of transcription 1 (STAT1) is the key transcriptional factor in IFN- signalling. Retinoic acid-inducible gene-I (RIG-I) is a member of the DExH box family of proteins and designated a putative RNA helicase. RNA helicases play diverse roles in regulation of gene expression and cellular functions, and RIG-I is implicated in antiviral responses.

The aim of the present study was to investigate the effect of IFN- on RIG-I expression in a cell line derived from human bronchial epithelial cells, BEAS-2B.

Induction of RIG-I in response to IFN- was found in BEAS-2B cells. Induction of RIG-I by IFN- was also demonstrated in another pulmonary epithelial cell line, NCI-H292. Transfection of BEAS-2B cells with RIG-I complementary DNA resulted in the upregulation of STAT1. Induction of IFN--inducible protein 10 by IFN- was enhanced in the cells overexpressing RIG-I.

It is concluded that retinoic acid-inducible gene-I may play an important role in the regulation of immunological reactions in bronchial epithelial cells elicited by interferon-.