Premium
Effects of Endogenous and Exogenous Prostaglandin E 2 on the Proliferation and Differentiation of a Mouse Cementoblast Cell Line (OCCM‐30)
Author(s) -
Mada Y.,
Miyauchi M.,
Oka H.,
Kitagawa M.,
Sakamoto K.,
Iizuka S.,
Sato S.,
Noguchi K.,
Somerman M.J.,
Takata T.
Publication year - 2006
Publication title -
journal of periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.036
H-Index - 156
eISSN - 1943-3670
pISSN - 0022-3492
DOI - 10.1902/jop.2006.060148
Subject(s) - cementoblast , osteoprotegerin , bone sialoprotein , osteocalcin , rankl , alkaline phosphatase , medicine , endocrinology , chemistry , prostaglandin e , dental cementum , cellular differentiation , cell growth , receptor , activator (genetics) , microbiology and biotechnology , cementum , biology , enzyme , biochemistry , dentin , gene , pathology
Background: Cementum formation is considered to be a critical event for successful regeneration of periodontal tissues. Cementoblasts share many characteristics with osteoblasts. Prostaglandin E 2 (PGE 2 ) is an important local factor in bone metabolism. Although the effects of PGE 2 on osteoblasts are well known, its effects on cementoblasts have not yet been established. We examined the effects of PGE 2 on proliferation and differentiation in a mouse cementoblast cell line, OCCM‐30 cells. Methods: OCCM‐30 cells were treated with three concentrations of PGE 2 (10, 100, and 1,000 ng/ml). Cell number, alkaline phosphatase (ALP) activity, and expression for mineralization‐related genes were determined. Osteoprotegerin (OPG) and receptor activator of nuclear factor‐kappa B (NF‐κB) ligand (RANKL) expression were also examined by real‐time polymerase chain reaction (RT‐PCR) and enzyme‐linked immunosorbent assay (ELISA). Results: The addition of PGE 2 at the highest dose used in this study suppressed cell proliferation of OCCM‐30 cells. The expression of mineralization‐related marker mRNA, such as type 1 collagen, ALP, bone sialoprotein (BSP), and osteocalcin (OCN), was constitutively detected in OCCM‐30 cells. PGE 2 dose dependently stimulated ALP activity and BSP‐mRNA expression in OCCM‐30 cells at day 3. Transcripts for OPG and RANKL and the protein level of OPG in culture media were upregulated with PGE 2 stimulation. Conclusion: These results demonstrate that PGE 2 suppressed cementoblast proliferation but stimulated ALP activity and the BSP‐mRNA level, suggesting a role of PGE 2 in controlling cementoblast differentiation, and further indicate that PGE 2 modulates RANKL and OPG expression in cementoblasts; the increase of OPG secreted from cementoblasts with PGE 2 stimulation may be essential to protect the root surface from resorption.