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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, KW2
Cai, J2
Kim, HY4
Hosoya, A1
Ohshima, H3
Choi, KY4
Jung, HS2
 
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
2012 Impact Factor: 2.123
2012 SCImago Journal Rankings: 0.917
 
DOIhttp://dx.doi.org/10.1002/jez.b.21309
 
ReferencesReferences in Scopus
 
DC FieldValue
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
2012 Impact Factor: 2.123
2012 SCImago Journal Rankings: 0.917
 
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
 
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<contributor.author>Ohshima, H</contributor.author>
<contributor.author>Choi, KY</contributor.author>
<contributor.author>Jung, HS</contributor.author>
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Author Affiliations
  1. Matsumoto Dental University
  2. Research Center for Orofacial Hard Tissue Regeneration
  3. Niigata University School of Medicine
  4. Yonsei University