Premium
TGF‐β1 and FGF2 Stimulate the Epithelial–Mesenchymal Transition of HERS Cells Through a MEK‐Dependent Mechanism
Author(s) -
Chen Jie,
Chen Guoqing,
Yan Zhiling,
Guo Yongwen,
Yu Mei,
Feng Lian,
Jiang Zongting,
Guo Weihua,
Tian Weidong
Publication year - 2014
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.24610
Subject(s) - epithelial–mesenchymal transition , microbiology and biotechnology , cementoblast , fibroblast growth factor , chemistry , transforming growth factor , periodontal fiber , cementum , mapk/erk pathway , mesenchymal stem cell , cancer research , biology , signal transduction , transition (genetics) , receptor , medicine , pathology , biochemistry , dentistry , dentin , gene
Hertwig’s epithelial root sheath (HERS) cells participate in cementum formation through epithelial–mesenchymal transition (EMT). Previous studies have shown that transforming growth factor beta 1 (TGF‐β1) and fibroblast growth factor 2 (FGF2) are involved in inducing EMT. However, their involvement in HERS cell transition remains elusive. In this study, we confirmed that HERS cells underwent EMT during the formation of acellular cementum. We found that both TGF‐β1 and FGF2 stimulated the EMT of HERS cells. The TGF‐β1 regulated the differentiation of HERS cells into periodontal ligament fibroblast‐like cells, and FGF2 directed the differentiation of HERS cells into cementoblast‐like cells. Treatment with TGF‐β1 or FGF2 inhibitor could effectively suppress HERS cells differential transition. Combined stimulation with both TGF‐β1 and FGF‐2 did not synergistically accelerate the EMT of HERS. Moreover, TGF‐β1/FGF2‐mediated EMT of HERS cells was reversed by the MEK1/2 inhibitor U0126. These results suggest that TGF‐β1 and FGF2 induce the EMT of HERS through a MAPK/ERK‐dependent signaling pathway. They also exert their different tendency of cellular differentiation during tooth root formation. This study further expands our knowledge of tooth root morphogenesis and provides more evidence for the use of alternative cell sources in clinical treatment of periodontal diseases. J. Cell. Physiol. 229: 1647–1659, 2014. © 2014 Wiley Periodicals, Inc.