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ERK activation is involved in tooth development via FGF10 signaling

Authors
 KYOUNG-WON CHO  ;  JINGLEI CAI  ;  HYUN-YI KIM  ;  AKIHIRO HOSOYA  ;  HAYATO OHSHIMA  ;  KANG-YELL CHOI  ;  HAN-SUNG JUNG 
Citation
 JOURNAL OF EXPERIMENTAL ZOOLOGY PART B-MOLECULAR AND DEVELOPMENTAL EVOLUTION, Vol.312(8) : 901-911, 2009 
Journal Title
 JOURNAL OF EXPERIMENTAL ZOOLOGY PART B-MOLECULAR AND DEVELOPMENTAL EVOLUTION 
ISSN
 1552-5007 
Issue Date
2009
MeSH
Animals ; Blotting, Western ; Enzyme Activation ; Extracellular Signal-Regulated MAP Kinases/metabolism* ; Fibroblast Growth Factor 10/metabolism* ; Immunohistochemistry ; Mice ; Mice, Nude ; Microscopy, Electron, Transmission ; Signal Transduction* ; Tooth/growth & development*
Abstract
The tooth is one of the ectodermal organs that develop from epithelial-mesenchymal interactions during embryonic development. An understanding of the underlying molecular mechanisms would improve our knowledge of the growth factors that regulate cell proliferation and differentiation. One of the related aspects is mitogen-activated protein kinase (MAPK) signaling in tooth differentiation. The extracellular-signal regulated kinase (ERK)/mitogen-activated protein kinase kinase (MEK) cascade plays a pivotal role in many of the essential cellular processes underlying embryonic development, including responses to major developmental changes. However, the role of the ERK pathway in molar development is unclear. This study investigated epithelial patterning and tooth growth in the mouse embryo by monitoring ERK and fibroblast growth factor (FGF) signaling. ERK, MEK, and phosphatase and tensin homolog (PTEN) were activated at different levels and locations in the developing tooth at E13.5 to E16.5 and PN2. ERK was activated in the inner dental epithelium and cervical loop, while PTEN was activated in the outer dental epithelium. In addition, only ERK was activated in secretory ameloblast at PN2. To further define the pathways involving FGF and ERK, tooth germs were cultured in the presence of compounds to inhibit MAPK/ERK-mediated signaling. Western blot analysis indicated that pERK2 was strongly activated in the tooth germ. Moreover, the activation level of pERK1 was dramatically increased by exogenous FGF10 alone and by combined treatment with FGF10 and U0126. The reported results will improve our understanding of the unique developmental processes of the dental epithelium and tooth growth, and will help to elucidate the fundamental mechanisms of ERK signaling underlying tooth development.
Full Text
http://onlinelibrary.wiley.com/doi/10.1002/jez.b.21309/abstract
DOI
10.1002/jez.b.21309
Appears in Collections:
2. College of Dentistry (치과대학) > Dept. of Oral Biology (구강생물학교실) > 1. Journal Papers
Yonsei Authors
Jung, Han Sung(정한성) ORCID logo https://orcid.org/0000-0003-2795-531X
Cho, Kyoung Won(조경원)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/105511
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