title: Aging of in vitro pulp illustrates change of inflammation and dentinogenesis.
abstract: BACKGROUND
  Dental pulp functions include pulp cell activity involvement in dentin formation. In this study we investigated the age-related changes in dental pulp cells that may influence pulp cell activity for restoring pulp function.
  
  
  METHODS
  Human dental pulp cells (HDPCs) were serially subcultured until spontaneously arrested. Altered expression of chronic inflammatory molecules and age-related molecules were determined by Western blotting. Odontogenic functions impaired by senescence were assayed by Western blotting, reverse transcriptase polymerase chain reaction, alkaline phosphatase activity, and alizarin red S staining. To understand the mechanism of aging process by stress-induced premature senescence (SIPS), the cells were treated with H(2)O(2). Replicative senescence and SIPS were also compared.
  
  
  RESULTS
  Replicative senescence of HDPCs was characterized by senescence-associated β-galactosidase activity and reactive oxygen species formation. These cells exhibited altered expression of chronic inflammatory molecules such as intracellular adhesion molecule-1, vascular cell adhesion molecule-1, peroxisome proliferator activated receptor-gamma, and heme oxygenase-1 and age-related molecules such as p53, p21, phosphorylated-extracellular signal-regulated kinase, and c-myb. SIPS cell results were similar to replicative senescence. Furthermore, HDPCs decreased odontogenic markers such as dentin sialophosphoprotein and dentin matrix-1 and osteogenic markers such as bone morphogenetic protein-2 and -7, runt-related transcription factor-2, osteopontin, alkaline phosphatase activity, and mineralized nodule formation by replicative senescence and SIPS.
  
  
  CONCLUSIONS
  This study suggests that development of aging-related molecules in pulp cells offers understanding of cellular mechanisms and biological events responsible for tooth preservation and maintenance strategies for healthy teeth across the life span.
authors: Department of Oral Biochemistry, Institute of Oral Bioscience, BK21 program, School of Dentistry, Chonbuk National University, Jeonju, Korea.
authors: Young-Hee
authors: YH
authors: Lee
authors: Go-Eun
authors: GE
authors: Kim
authors: Hye-Jin
authors: HJ
authors: Cho
authors: Mi-Kyoung
authors: MK
authors: Yu
authors: Govinda
authors: G
authors: Bhattarai
authors: Nan-Hee
authors: NH
authors: Lee
authors: Ho-Keun
authors: HK
authors: Yi
mesh_terms: D019588:Aging, Premature / Q000378:metabolism*; D019485:Bone Morphogenetic Proteins / Q000378:metabolism; D000075982:Cell Adhesion Molecule-1; D015815:Cell Adhesion Molecules / Q000096:biosynthesis; D002478:Cells, Cultured; D016922:Cellular Senescence / Q000502:physiology; D003782:Dental Pulp / Q000473:pathology* / Q000503:physiopathology; D003810:Dentinogenesis; D016326:Extracellular Matrix Proteins / Q000378:metabolism; D006801:Humans; D007136:Immunoglobulins / Q000096:biosynthesis; D010750:Phosphoproteins / Q000378:metabolism; D011671:Pulpitis / Q000378:metabolism* / Q000473:pathology; D017382:Reactive Oxygen Species / Q000378:metabolism; D012795:Sialoglycoproteins / Q000378:metabolism; D014074:Tooth Calcification; D019010:Vascular Cell Adhesion Molecule-1 / Q000096:biosynthesis; D001616:beta-Galactosidase / Q000378:metabolism; D000099311:Dentin Sialophosphoprotein
chemical_list: D019485:Bone Morphogenetic Proteins; D000075982:Cell Adhesion Molecule-1; D015815:Cell Adhesion Molecules; D016326:Extracellular Matrix Proteins; D007136:Immunoglobulins; D010750:Phosphoproteins; D017382:Reactive Oxygen Species; D012795:Sialoglycoproteins; D019010:Vascular Cell Adhesion Molecule-1; D001616:beta-Galactosidase; D000099311:Dentin Sialophosphoprotein; C403514:CADM1 protein, human; C513309:DMP1 protein, human