File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: MAPK mediates Hsp25 signaling in incisor development

TitleMAPK mediates Hsp25 signaling in incisor development
Authors
Issue Date2009
PublisherSpringer Verlag. The Journal's web site is located at http://link.springer.de/link/service/journals/00418/index.htm
Citation
Histochemistry And Cell Biology, 2009, v. 131 n. 5, p. 593-603 How to Cite?
Abstract
Rodent incisors are continuously growing teeth that include all stages of amelogenesis. Understanding amelogenesis requires investigations of the genes and their gene products control the ameloblast phenotype. One of the mechanisms related to tooth differentiation is mitogen-activated protein kinase (MAPK) signaling. The extracellular-signal regulated kinase (ERK)/mitogen-activated protein kinase kinase (MEK) cascade is associated with mechanisms that control the cell cycle and cell survival. However, the roles of cascades in incisor development remain to be determined. In this study, we investigated incisor development and growth in the mouse based on MAPK signaling. Moreover, heat-shock protein (Hsp)-25 is well known to be a useful marker of odontoblast differentiation. We used anisomycin (a protein-synthesis inhibitor that activates MAPKs) and U0126 (a MAPK inhibitor that blocks ERK1/2 phosphorylation) to examine the role of MAPKs in Hsp25 signaling in the development of the mouse incisor. We performed immunohistochemistry and in vitro culture using incisor tooth germ, and found that phospho-ERK (pERK), pMEK, and Hsp25 localized in developing incisor ameloblasts and anisomycin failed to produce incisor development. In addition, Western blotting results showed that anisomycin stimulated the phosphorylation of ERK, MEK, and Hsp25, and that some of these proteins were blocked by the U0126. These findings suggest that MAPK signals play important roles in incisor formation, differentiation, and development by mediating Hsp25 signaling. © 2009 Springer-Verlag.
Persistent Identifierhttp://hdl.handle.net/10722/169558
ISSN
2013 Impact Factor: 2.927
ISI Accession Number ID
References

 

Author Affiliations
  1. Yonsei University
  2. Iwate Medical University
DC FieldValueLanguage
dc.contributor.authorLee, MJen_US
dc.contributor.authorCai, Jen_US
dc.contributor.authorKwak, SWen_US
dc.contributor.authorCho, SWen_US
dc.contributor.authorHarada, Hen_US
dc.contributor.authorJung, HSen_US
dc.date.accessioned2012-10-25T04:52:51Z-
dc.date.available2012-10-25T04:52:51Z-
dc.date.issued2009en_US
dc.identifier.citationHistochemistry And Cell Biology, 2009, v. 131 n. 5, p. 593-603en_US
dc.identifier.issn0948-6143en_US
dc.identifier.urihttp://hdl.handle.net/10722/169558-
dc.description.abstractRodent incisors are continuously growing teeth that include all stages of amelogenesis. Understanding amelogenesis requires investigations of the genes and their gene products control the ameloblast phenotype. One of the mechanisms related to tooth differentiation is mitogen-activated protein kinase (MAPK) signaling. The extracellular-signal regulated kinase (ERK)/mitogen-activated protein kinase kinase (MEK) cascade is associated with mechanisms that control the cell cycle and cell survival. However, the roles of cascades in incisor development remain to be determined. In this study, we investigated incisor development and growth in the mouse based on MAPK signaling. Moreover, heat-shock protein (Hsp)-25 is well known to be a useful marker of odontoblast differentiation. We used anisomycin (a protein-synthesis inhibitor that activates MAPKs) and U0126 (a MAPK inhibitor that blocks ERK1/2 phosphorylation) to examine the role of MAPKs in Hsp25 signaling in the development of the mouse incisor. We performed immunohistochemistry and in vitro culture using incisor tooth germ, and found that phospho-ERK (pERK), pMEK, and Hsp25 localized in developing incisor ameloblasts and anisomycin failed to produce incisor development. In addition, Western blotting results showed that anisomycin stimulated the phosphorylation of ERK, MEK, and Hsp25, and that some of these proteins were blocked by the U0126. These findings suggest that MAPK signals play important roles in incisor formation, differentiation, and development by mediating Hsp25 signaling. © 2009 Springer-Verlag.en_US
dc.languageengen_US
dc.publisherSpringer Verlag. The Journal's web site is located at http://link.springer.de/link/service/journals/00418/index.htmen_US
dc.relation.ispartofHistochemistry and Cell Biologyen_US
dc.subject.meshAmeloblasts - Cytology - Drug Effects - Metabolismen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAnisomycin - Pharmacologyen_US
dc.subject.meshButadienes - Pharmacologyen_US
dc.subject.meshCell Lineen_US
dc.subject.meshExtracellular Signal-Regulated Map Kinases - Drug Effects - Metabolismen_US
dc.subject.meshHeat-Shock Proteins - Drug Effects - Metabolismen_US
dc.subject.meshIncisor - Drug Effects - Growth & Development - Metabolismen_US
dc.subject.meshKi-67 Antigen - Drug Effects - Metabolismen_US
dc.subject.meshMap Kinase Kinase Kinases - Drug Effects - Metabolismen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Inbred Icren_US
dc.subject.meshNeoplasm Proteins - Drug Effects - Metabolismen_US
dc.subject.meshNitriles - Pharmacologyen_US
dc.subject.meshOrgan Culture Techniquesen_US
dc.subject.meshRatsen_US
dc.subject.meshSignal Transduction - Drug Effects - Physiologyen_US
dc.titleMAPK mediates Hsp25 signaling in incisor developmenten_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.doi10.1007/s00418-009-0568-2en_US
dc.identifier.pmid19225803en_US
dc.identifier.scopuseid_2-s2.0-63949085382en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-63949085382&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume131en_US
dc.identifier.issue5en_US
dc.identifier.spage593en_US
dc.identifier.epage603en_US
dc.identifier.isiWOS:000264811100006-
dc.publisher.placeGermanyen_US
dc.identifier.scopusauthoridLee, MJ=35264472100en_US
dc.identifier.scopusauthoridCai, J=9246458800en_US
dc.identifier.scopusauthoridKwak, SW=7202607781en_US
dc.identifier.scopusauthoridCho, SW=32967447200en_US
dc.identifier.scopusauthoridHarada, H=7402619046en_US
dc.identifier.scopusauthoridJung, HS=7403030195en_US
dc.identifier.citeulike4088213-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats