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J. Biol. Chem., Vol. 278, Issue 26, 23243-23250, June 27, 2003

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Interleukin-1 and Tumor Necrosis Factor- Induce MUC5AC Overexpression through a Mechanism Involving ERK/p38 Mitogen-activated Protein Kinases-MSK1-CREB Activation in Human Airway Epithelial Cells^*

Kyoung Seob Song , Won-Jae Lee , Kwang Chul Chung ¶, Ja Seok Koo || **, Eun Jin Yang ¶, Jae Young Choi  and Joo-Heon Yoon   

From the Brain Korea 21 Project for Medical Sciences, Yonsei University College of Medicine, Seoul 120-752, the Division of Molecular Life Science, Ewha Womans University, Seoul 120-750, the^¶Department of Biology, College of Sciences, Yonsei University, Seoul 120-749, Korea, the ^||Department of Thoracic/Head and Neck Medical Oncology, M. D. Anderson Cancer Center, University of Texas, Houston, Texas 77030-4009, and the Department of Otorhinolaryngology, Yonsei University College of Medicine, Seoul 120-752, Korea

Mucin hypersecretion is commonly observed in many inflammatory diseases of the respiratory tract. MUC5AC is generally recognized to be a major airway mucin because MUC5AC is highly expressed in the goblet cells of human airway epithelium. Moreover, it is regulated by various inflammatory cytokines. However, the mechanisms by which the interleukin (IL)-1 and tumor necrosis factor (TNF)- induce MUC5AC gene expression in normal nasal epithelial cells, and the signal molecules involved, especially in the downstream signaling of mitogen-activated protein (MAP) kinases, remain unclear. Here we show that pharmacologic or genetic inhibition of either ERK or p38 MAP kinase pathway abolished IL-1- and TNF--induced MUC5AC gene expression in normal human nasal epithelial cells. Our results also indicate that the activation of mitogen- and stress-activated protein kinase 1 (MSK1) and cAMP-response element-binding protein and cAMP-response element signaling cascades via ERK and p38 MAP kinases are crucial aspects of the intracellular mechanisms that mediate MUC5AC gene expression. Taken together, these studies give additional insights into the molecular mechanism of IL-1- and TNF--induced MUC5AC gene expression and enhance our understanding on mucin hypersecretion during inflammation.

Received for publication, January 6, 2003

^* This work was supported by Grant 02-PJ1-PG3-20908-0005 from 2002 Good HealthR&D Project, Ministry of Health and Welfare, South Korea. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

^** Supported by United States Public Health Service Grant K22 ESOO3662-01 from the NIEHS, National Institutes of Health.

To whom correspondence should be addressed: Dept. of Otorhinolaryngology, Yonsei University College of Medicine, 134 Shinchon-dong, Seodaemun-gu, Seoul, 120-752, Korea. Tel.: 82-2-361-8484; Fax: 82-2-393-0580; E-mail: jhyoon{at}yumc.yonsei.ac.kr.

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