title: Activation of the Notch signaling pathway in response to pulp capping of rat molars.
abstract: Notch signaling is an evolutionarily conserved pathway that controls the developmental choices made by individual cells. Cells communicate via Notch receptors and their ligands, which direct decisions on the fate of stem cells according to the states of their neighbors. In this study we explored Notch signaling after the pulp capping of adult first upper rat molars. The wound was capped with calcium hydroxide. In situ hybridization revealed an increased expression of Notch signaling genes on day 1, which showed a tendency to decrease on day 3. Notch1 increased in the subodontoblast zone and close to the lesion limited to a few cells. Notch2 increased in pulp stroma surrounded by coronal odontoblasts. Notch1 and, especially, Notch3 expression increased, corresponding to perivascular cell groups. A low increase of ligand expression was observed near the injury with Delta1 expression along the dentin wall and Jagged1 in the stroma. Expression of the downstream target, Hes1, was observed along the lesion and adjacent dentin walls. Hes5 expression was not observed. The results indicate that Notch signaling is activated in response to injury and associated with the differentiation of pulp cells into perivascular cells and odontoblasts. The findings are consistent with the concept that the Notch pathway controls stem cell fate during pulp regeneration.
authors.affiliation: Department of Dental Pathology, Operative Dentistry and Endodontics, Royal Dental College, Faculty of Health Sciences, University of Aarhus, Denmark. loev@odont.au.dk
authors.forename: H
authors.initials: H
authors.lastname: Løvschall
authors.forename: M
authors.initials: M
authors.lastname: Tummers
authors.forename: I
authors.initials: I
authors.lastname: Thesleff
authors.forename: E-M
authors.initials: EM
authors.lastname: Füchtbauer
authors.forename: K
authors.initials: K
authors.lastname: Poulsen
mesh_terms: D000818:Animals; D051792:Basic Helix-Loop-Helix Proteins / Q000378:metabolism; D003782:Dental Pulp / Q000166:cytology / Q000293:injuries / Q000378:metabolism*; D003785:Dental Pulp Capping; D018398:Homeodomain Proteins / Q000378:metabolism; D047908:Intracellular Signaling Peptides and Proteins; D008297:Male; D008437:Maxilla; D008565:Membrane Proteins / Q000378:metabolism; D008963:Molar; D051381:Rats; D017208:Rats, Wistar; D051881:Receptor, Notch1 / Q000378:metabolism; D051883:Receptor, Notch2 / Q000378:metabolism*; D000071656:Receptor, Notch3; D051880:Receptors, Notch / Q000378:metabolism*; D015398:Signal Transduction / Q000502:physiology*; D013234:Stem Cells / Q000378:metabolism*; D018677:Tooth Injuries / Q000378:metabolism; D000072056:Transcription Factor HES-1; D015854:Up-Regulation
chemical_list: D051792:Basic Helix-Loop-Helix Proteins; D018398:Homeodomain Proteins; D047908:Intracellular Signaling Peptides and Proteins; D008565:Membrane Proteins; D051881:Receptor, Notch1; D051883:Receptor, Notch2; D000071656:Receptor, Notch3; D051880:Receptors, Notch; D000072056:Transcription Factor HES-1; C489735:Hes1 protein, rat; C497763:Notch1 protein, rat; C497766:Notch2 protein, rat; C498556:Notch3 protein, rat; C064045:delta protein