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- Publisher Website: 10.1007/s00418-009-0568-2
- Scopus: eid_2-s2.0-63949085382
- PMID: 19225803
- WOS: WOS:000264811100006
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Article: MAPK mediates Hsp25 signaling in incisor development
Title | MAPK mediates Hsp25 signaling in incisor development |
---|---|
Authors | |
Keywords | Ameloblasts Differentiation Hsp25 Incisor MAPK signaling |
Issue Date | 2009 |
Publisher | Springer 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 Identifier | http://hdl.handle.net/10722/169558 |
ISSN | 2023 Impact Factor: 2.1 2023 SCImago Journal Rankings: 0.712 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Lee, MJ | en_US |
dc.contributor.author | Cai, J | en_US |
dc.contributor.author | Kwak, SW | en_US |
dc.contributor.author | Cho, SW | en_US |
dc.contributor.author | Harada, H | en_US |
dc.contributor.author | Jung, HS | en_US |
dc.date.accessioned | 2012-10-25T04:52:51Z | - |
dc.date.available | 2012-10-25T04:52:51Z | - |
dc.date.issued | 2009 | en_US |
dc.identifier.citation | Histochemistry And Cell Biology, 2009, v. 131 n. 5, p. 593-603 | en_US |
dc.identifier.issn | 0948-6143 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/169558 | - |
dc.description.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. | en_US |
dc.language | eng | en_US |
dc.publisher | Springer Verlag. The Journal's web site is located at http://link.springer.de/link/service/journals/00418/index.htm | en_US |
dc.relation.ispartof | Histochemistry and Cell Biology | en_US |
dc.subject | Ameloblasts | - |
dc.subject | Differentiation | - |
dc.subject | Hsp25 | - |
dc.subject | Incisor | - |
dc.subject | MAPK signaling | - |
dc.subject.mesh | Ameloblasts - Cytology - Drug Effects - Metabolism | en_US |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | Anisomycin - Pharmacology | en_US |
dc.subject.mesh | Butadienes - Pharmacology | en_US |
dc.subject.mesh | Cell Line | en_US |
dc.subject.mesh | Extracellular Signal-Regulated Map Kinases - Drug Effects - Metabolism | en_US |
dc.subject.mesh | Heat-Shock Proteins - Drug Effects - Metabolism | en_US |
dc.subject.mesh | Incisor - Drug Effects - Growth & Development - Metabolism | en_US |
dc.subject.mesh | Ki-67 Antigen - Drug Effects - Metabolism | en_US |
dc.subject.mesh | Map Kinase Kinase Kinases - Drug Effects - Metabolism | en_US |
dc.subject.mesh | Mice | en_US |
dc.subject.mesh | Mice, Inbred Icr | en_US |
dc.subject.mesh | Neoplasm Proteins - Drug Effects - Metabolism | en_US |
dc.subject.mesh | Nitriles - Pharmacology | en_US |
dc.subject.mesh | Organ Culture Techniques | en_US |
dc.subject.mesh | Rats | en_US |
dc.subject.mesh | Signal Transduction - Drug Effects - Physiology | en_US |
dc.title | MAPK mediates Hsp25 signaling in incisor development | en_US |
dc.type | Article | en_US |
dc.identifier.email | Jung, HS: hsjung@yuhs.ac | en_US |
dc.identifier.authority | Jung, HS=rp01683 | en_US |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.doi | 10.1007/s00418-009-0568-2 | en_US |
dc.identifier.pmid | 19225803 | - |
dc.identifier.scopus | eid_2-s2.0-63949085382 | en_US |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-63949085382&selection=ref&src=s&origin=recordpage | en_US |
dc.identifier.volume | 131 | en_US |
dc.identifier.issue | 5 | en_US |
dc.identifier.spage | 593 | en_US |
dc.identifier.epage | 603 | en_US |
dc.identifier.isi | WOS:000264811100006 | - |
dc.publisher.place | Germany | en_US |
dc.identifier.scopusauthorid | Lee, MJ=35264472100 | en_US |
dc.identifier.scopusauthorid | Cai, J=9246458800 | en_US |
dc.identifier.scopusauthorid | Kwak, SW=7202607781 | en_US |
dc.identifier.scopusauthorid | Cho, SW=32967447200 | en_US |
dc.identifier.scopusauthorid | Harada, H=7402619046 | en_US |
dc.identifier.scopusauthorid | Jung, HS=7403030195 | en_US |
dc.identifier.citeulike | 4088213 | - |
dc.identifier.issnl | 0948-6143 | - |