title: Dental follicle cells and cementoblasts induce apoptosis of ameloblast-lineage and Hertwig's epithelial root sheath/epithelial rests of Malassez cells through the Fas-Fas ligand pathway.
abstract: Hertwig's epithelial root sheath (HERS), epithelial rests of Malassez (ERM) cells, and reduced ameloblasts undergo apoptosis during tooth development. This study examined the effects of dental follicle cells and cementoblasts on the apoptosis of ameloblast-lineage and HERS/ERM cells derived from the enamel organ. We also elucidated the induction pathways and identified the apoptotic pathway involved in this process. Here, we showed terminal deoxynucleotidyl transferase-mediated biotin-dUTP nick-end labeling (TUNEL)-positive HERS cells and reduced ameloblasts near dental follicle cells during tooth development. Co-culturing ameloblast-lineage cell line (ALC) ameloblasts and HERS/ERM cells with either dental follicle cells or OCCM-30 cementoblasts markedly enhanced the apoptosis of ameloblasts and HERS/ERM cells compared with cells cultured alone. However, dental follicle cells and cementoblasts did not modulate the apoptotic responses of co-cultured non-odontogenic MCF10A or KB cells. When ameloblasts + HERS and cementoblasts + dental follicle cells were co-cultured, the expression of Fas ligand (FasL) increased in cementoblasts + dental follicle cells, while the expression of Fas increased in ameloblasts + HERS. Interestingly, recombinant FasL induced ameloblast apoptosis while the cementoblast-induced ameloblast apoptosis was suppressed by the Fas/FasL antagonist Kp7-6. These results suggest that during tooth development, dental follicle cells and cementoblasts induce apoptosis of ameloblast-lineage and HERS/ERM cells through the Fas-FasL pathway, but do not induce the apoptosis of non-odontogenic epithelial cells.
authors.affiliation: Department of Oral Histology-Developmental Biology & Dental Research Institute, BK21 Project, School of Dentistry, Seoul National University, Seoul, South Korea.
authors.forename: Ji-Hyun
authors.initials: JH
authors.lastname: Lee
authors.forename: Dong-Seol
authors.initials: DS
authors.lastname: Lee
authors.forename: Hyun
authors.initials: H
authors.lastname: Nam
authors.forename: Gene
authors.initials: G
authors.lastname: Lee
authors.forename: Byoung-Moo
authors.initials: BM
authors.lastname: Seo
authors.forename: Young-Sik
authors.initials: YS
authors.lastname: Cho
authors.forename: Hyun-Sook
authors.initials: HS
authors.lastname: Bae
authors.forename: Joo-Cheol
authors.initials: JC
authors.lastname: Park
mesh_terms: D000293:Adolescent; D000565:Ameloblasts / Q000502:physiology*; D017209:Apoptosis / Q000502:physiology*; D015153:Blotting, Western; D018929:Cell Culture Techniques; D019070:Cell Lineage; D048430:Cell Shape; D002478:Cells, Cultured; D018920:Coculture Techniques; D020552:Comet Assay; D053938:DNA Fragmentation; D003739:Dental Cementum / Q000502:physiology*; D003795:Dental Sac / Q000166:cytology* / Q000502:physiology; D004658:Enamel Organ / Q000166:cytology* / Q000502:physiology; D004847:Epithelial Cells / Q000502:physiology; D053222:Fas Ligand Protein / Q000037:antagonists & inhibitors / Q000502:physiology*; D005347:Fibroblasts / Q000502:physiology; D005434:Flow Cytometry; D006801:Humans; D020287:In Situ Nick-End Labeling; D009805:Odontogenesis / Q000502:physiology; D010513:Periodontal Ligament / Q000166:cytology* / Q000502:physiology; D015398:Signal Transduction / Q000502:physiology; D014092:Tooth Root / Q000166:cytology* / Q000502:physiology; D055815:Young Adult; D019014:fas Receptor / Q000037:antagonists & inhibitors / Q000502:physiology*
chemical_list: C491901:FAS protein, human; D053222:Fas Ligand Protein; D019014:fas Receptor