Original Article
Copyright ©2013 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Exp Med. Nov 20, 2013; 3(4): 100-107
Published online Nov 20, 2013. doi: 10.5493/wjem.v3.i4.100
Epigallocatechin-3-gallate suppresses transforming growth factor-beta signaling by interacting with the transforming growth factor-beta type II receptor
Masaki Tabuchi, Sumio Hayakawa, Eiko Honda, Kana Ooshima, Tatsuki Itoh, Koji Yoshida, Ah-Mee Park, Hideaki Higashino, Mamoru Isemura, Hiroshi Munakata
Masaki Tabuchi, Koji Yoshida, Ah-Mee Park, Hiroshi Munakata, Department of Biochemistry, Kinki University Faculty of Medicine, Osaka-Sayama 589-8511, Japan
Sumio Hayakawa, Division of Signaling in Cancer and Immunology, Institute for Genetic Medicine, Hokkaido University, Sapporo 060-0815, Japan
Eiko Honda, Life Science Research Institute, Kinki University, Osaka-Sayama 589-8511, Japan
Kana Ooshima, Hideaki Higashino, Department of Pharmacology, Kinki University Faculty of Medicine, Osaka-Sayama 589-8511, Japan
Tatsuki Itoh, Department of Pathology, Kinki University Faculty of Medicine, Osaka-Sayama 589-8511, Japan
Mamoru Isemura, Graduate School of Nutritional and Environmental Sciences, University of Shizuoka, Shizuoka 422-8526, Japan
Author contributions: Tabuchi M and Hayakawa S contributed equally to this work; Tabuchi M and Hayakawa S designed studies; Tabuchi M, Hayakawa S, Honda E, Ooshima K, Itoh T, Yoshida K, Park AM, Higashino H and Isemura M performed the research; Tabuchi M, Hayakawa S and Munakata H analyzed the data; Munakata H wrote the paper.
Correspondence to: Hiroshi Munakata, Professor, Department of Biochemistry, Kinki University Faculty of Medicine, 377-2 Ohnohigashi, Osaka-Sayama 589-8511, Japan. munakata@med.kindai.ac.jp
Telephone: +81-72-3660221 Fax: +81-72-3660245
Received: May 14, 2013
Revised: July 12, 2013
Accepted: September 18, 2013
Published online: November 20, 2013
Core Tip

Core tip: (-)-Epigallocatechin-3-gallate (EGCG) binds to transforming growth factor-β (TGF-β) type II receptor (TGFRII) and inhibits TGF-β action by interfering with the interaction between TGF-β and TGFRII. Because TGF-β is considered to be the strongest inducer of tissue fibrosis, the obtained data from this investigation suggest that EGCG may be a new therapeutic agent for organ fibrosis.