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International Journal of Otolaryngology
Volume 2012, Article ID 438609, 5 pages
Review Article

The Role of Atoh1 in Mucous Cell Metaplasia

1Department of Otolaryngology, Nagoya City University School of Medicine, 1 Kawasumi Mizuho-cho, Mizuho-ku, Nagoya, Aichi 467-8601, Japan
2Department of Otolaryngology, Kochi University School of Medicine, 2-5-1 Akebono-cho, Kochi 780-8520, Japan
3Department of Otolaryngology, University of Minnesota School of Medicine, 2001 6th Street SE, Minneapolis, MN 55455, USA

Received 10 September 2011; Accepted 8 November 2011

Academic Editor: Per Cayé-Thomasen

Copyright © 2012 Yoshihisa Nakamura et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


A key issue in otitis media is mucous cell metaplasia which is responsible for mucous hypersecretion and persistence of the disease. However, little is known about the molecular mechanisms of mucous cell metaplasia in otitis media. Numerous studies of intestinal epithelial homeostasis have shown that Atonal homolog 1 (Atoh1), a basic helix-loop-helix (bHLH) transcription factor, is essential for the intestinal goblet cell differentiation. On the other hand, SAM-pointed domain-containing Ets transcription factor (SPDEF), a member of the “Ets” transcription factor family, has been reported to trigger the mucous cell metaplasia of pulmonary infectious diseases or athsma. Recent studies have demonstrated the relation of these factors, that is, Spdef functions downstream of Atoh1. We could take the adventages of these findings for the study of otitis media because both middle ear and pulmonary epithelia belong to the same respiratory tract. Atoh1 and SPDEF could be the therapeutic targets for otitis media associated with mucous cell metaplasia which is frequently considered “intractable” in the clinical settings.