title: MAPK mediates Hsp25 signaling in incisor development.
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.
authors.affiliation: Department of Oral Biology, College of Dentistry, Yonsei Center of Biotechnology, Yonsei University, 134 Shinchon-Dong, Seodaemoon-Gu, Seoul, 120-752, Korea.
authors.forename: Min-Jung
authors.initials: MJ
authors.lastname: Lee
authors.forename: Jinglei
authors.initials: J
authors.lastname: Cai
authors.forename: Sung-Wook
authors.initials: SW
authors.lastname: Kwak
authors.forename: Sung-Won
authors.initials: SW
authors.lastname: Cho
authors.forename: Hidemitsu
authors.initials: H
authors.lastname: Harada
authors.forename: Han-Sung
authors.initials: HS
authors.lastname: Jung
mesh_terms: D000565:Ameloblasts / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D000818:Animals; D000841:Anisomycin / Q000494:pharmacology; D002070:Butadienes / Q000494:pharmacology; D002460:Cell Line; D048049:Extracellular Signal-Regulated MAP Kinases / Q000187:drug effects / Q000378:metabolism*; D006360:Heat-Shock Proteins / Q000187:drug effects / Q000378:metabolism*; D007180:Incisor / Q000187:drug effects / Q000254:growth & development* / Q000378:metabolism; D019394:Ki-67 Antigen / Q000187:drug effects / Q000378:metabolism; D020930:MAP Kinase Kinase Kinases / Q000187:drug effects / Q000378:metabolism*; D051379:Mice; D008813:Mice, Inbred ICR; D018832:Molecular Chaperones; D009363:Neoplasm Proteins / Q000187:drug effects / Q000378:metabolism*; D009570:Nitriles / Q000494:pharmacology; D009924:Organ Culture Techniques; D051381:Rats; D015398:Signal Transduction / Q000187:drug effects / Q000502:physiology
chemical_list: D002070:Butadienes; D006360:Heat-Shock Proteins; C486113:Hsbp1 protein, mouse; D019394:Ki-67 Antigen; D018832:Molecular Chaperones; D009363:Neoplasm Proteins; D009570:Nitriles; C113580:U 0126; D000841:Anisomycin; D048049:Extracellular Signal-Regulated MAP Kinases; D020930:MAP Kinase Kinase Kinases