Article: ERK activation is involved in tooth development via FGF10 signaling

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TitleERK activation is involved in tooth development via FGF10 signaling
AuthorsCho, KW1
Cai, J1
Kim, HY3
Hosoya, A2
Ohshima, H4
Choi, KY3
Jung, HS1
Issue Date2009
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.interscience.wiley.com/jpages/0022-104X:1/
CitationJournal Of Experimental Zoology Part B: Molecular And Developmental Evolution, 2009, v. 312 n. 8, p. 901-911 [How to Cite?]
DOI: http://dx.doi.org/10.1002/jez.b.21309
AbstractThe 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. © 2009 Wiley-Liss, Inc.
ISSN1552-5007
2011 Impact Factor: 2.416
2011 SCImago Journal Rankings: 0.280
DOIhttp://dx.doi.org/10.1002/jez.b.21309
ReferencesReferences in Scopus
DC Field
Value
dc.contributor.authorCho, KW
dc.contributor.authorCai, J
dc.contributor.authorKim, HY
dc.contributor.authorHosoya, A
dc.contributor.authorOhshima, H
dc.contributor.authorChoi, KY
dc.contributor.authorJung, HS
dc.date.accessioned2012-10-25T04:52:55Z
dc.date.available2012-10-25T04:52:55Z
dc.date.issued2009
dc.description.abstractThe 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. © 2009 Wiley-Liss, Inc.
dc.description.natureLink_to_subscribed_fulltext
dc.identifier.citationJournal Of Experimental Zoology Part B: Molecular And Developmental Evolution, 2009, v. 312 n. 8, p. 901-911 [How to Cite?]
DOI: http://dx.doi.org/10.1002/jez.b.21309
dc.identifier.doihttp://dx.doi.org/10.1002/jez.b.21309
dc.identifier.epage911
dc.identifier.issn1552-5007
2011 Impact Factor: 2.416
2011 SCImago Journal Rankings: 0.280
dc.identifier.issue8
dc.identifier.pmid19551815
dc.identifier.scopuseid_2-s2.0-70449106243
dc.identifier.spage901
dc.identifier.urihttp://hdl.handle.net/10722/169565
dc.identifier.volume312
dc.languageeng
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.interscience.wiley.com/jpages/0022-104X:1/
dc.publisher.placeUnited States
dc.relation.ispartofJournal of Experimental Zoology Part B: Molecular and Developmental Evolution
dc.relation.referencesReferences in Scopus
dc.subject.meshAnimals
dc.subject.meshBlotting, Western
dc.subject.meshEnzyme Activation
dc.subject.meshExtracellular Signal-Regulated Map Kinases - Metabolism
dc.subject.meshFibroblast Growth Factor 10 - Metabolism
dc.subject.meshImmunohistochemistry
dc.subject.meshMice
dc.subject.meshMice, Nude
dc.subject.meshMicroscopy, Electron, Transmission
dc.subject.meshSignal Transduction
dc.subject.meshTooth - Growth & Development
dc.titleERK activation is involved in tooth development via FGF10 signaling
dc.typeArticle
Author Affiliations
  1. Research Center for Orofacial Hard Tissue Regeneration
  2. Matsumoto Dental University
  3. Yonsei University
  4. Niigata University School of Medicine