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

TitleERK activation is involved in tooth development via FGF10 signaling
Authors
Issue Date2009
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.interscience.wiley.com/jpages/0022-104X:1/
Citation
Journal Of Experimental Zoology Part B: Molecular And Developmental Evolution, 2009, v. 312 n. 8, p. 901-911 How to Cite?
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. © 2009 Wiley-Liss, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/169565
ISSN
2013 Impact Factor: 1.876
ISI Accession Number ID
References

 

Author Affiliations
  1. Matsumoto Dental University
  2. Research Center for Orofacial Hard Tissue Regeneration
  3. Niigata University School of Medicine
  4. Yonsei University
DC FieldValueLanguage
dc.contributor.authorCho, KWen_US
dc.contributor.authorCai, Jen_US
dc.contributor.authorKim, HYen_US
dc.contributor.authorHosoya, Aen_US
dc.contributor.authorOhshima, Hen_US
dc.contributor.authorChoi, KYen_US
dc.contributor.authorJung, HSen_US
dc.date.accessioned2012-10-25T04:52:55Z-
dc.date.available2012-10-25T04:52:55Z-
dc.date.issued2009en_US
dc.identifier.citationJournal Of Experimental Zoology Part B: Molecular And Developmental Evolution, 2009, v. 312 n. 8, p. 901-911en_US
dc.identifier.issn1552-5007en_US
dc.identifier.urihttp://hdl.handle.net/10722/169565-
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.en_US
dc.languageengen_US
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.interscience.wiley.com/jpages/0022-104X:1/en_US
dc.relation.ispartofJournal of Experimental Zoology Part B: Molecular and Developmental Evolutionen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBlotting, Westernen_US
dc.subject.meshEnzyme Activationen_US
dc.subject.meshExtracellular Signal-Regulated Map Kinases - Metabolismen_US
dc.subject.meshFibroblast Growth Factor 10 - Metabolismen_US
dc.subject.meshImmunohistochemistryen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Nudeen_US
dc.subject.meshMicroscopy, Electron, Transmissionen_US
dc.subject.meshSignal Transductionen_US
dc.subject.meshTooth - Growth & Developmenten_US
dc.titleERK activation is involved in tooth development via FGF10 signalingen_US
dc.typeArticleen_US
dc.identifier.emailJung, HS: hsjung@yuhs.acen_US
dc.identifier.authorityJung, HS=rp01683en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1002/jez.b.21309en_US
dc.identifier.pmid19551815en_US
dc.identifier.scopuseid_2-s2.0-70449106243en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-70449106243&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume312en_US
dc.identifier.issue8en_US
dc.identifier.spage901en_US
dc.identifier.epage911en_US
dc.identifier.isiWOS:000271958800009-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridCho, KW=7403956665en_US
dc.identifier.scopusauthoridCai, J=9246458800en_US
dc.identifier.scopusauthoridKim, HY=36014754000en_US
dc.identifier.scopusauthoridHosoya, A=8651007100en_US
dc.identifier.scopusauthoridOhshima, H=7202879991en_US
dc.identifier.scopusauthoridChoi, KY=7403949379en_US
dc.identifier.scopusauthoridJung, HS=7403030195en_US

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