Effects of endogenous and exogenous prostaglandin E2 on the proliferation and differentiation of a mouse cementoblast cell line (OCCM-30).
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-kappaB) 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.


CONCLUSIONS
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.
Mada
Y
Y
Department of Oral Maxillofacial Pathobiology, Graduate School of Biomedical Sciences, Hiroshima University, Hiroshima, Japan.
Miyauchi
M
M
Oka
H
H
Kitagawa
M
M
Sakamoto
K
K
Iizuka
S
S
Sato
S
S
Noguchi
K
K
Somerman
M J
MJ
Takata
T
T
D000469:Alkaline Phosphatase / Q000235:genetics / Q000378:metabolism*; D000818:Animals; D002454:Cell Differentiation / Q000502:physiology*; D002460:Cell Line; D049109:Cell Proliferation; D025021:Cementogenesis / Q000502:physiology*; D003739:Dental Cementum / Q000166:cytology / Q000378:metabolism*; D015232:Dinoprostone / Q000008:administration & dosage / Q000502:physiology*; D004305:Dose-Response Relationship, Drug; D005786:Gene Expression Regulation; D058574:Integrin-Binding Sialoprotein; D051379:Mice; D015675:Osteocalcin / Q000235:genetics / Q000378:metabolism; D053244:Osteoprotegerin / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000032:analysis; D012795:Sialoglycoproteins / Q000235:genetics / Q000378:metabolism; D018709:Statistics, Nonparametric
C546872:Ibsp protein, mouse; D058574:Integrin-Binding Sialoprotein; D053244:Osteoprotegerin; D012333:RNA, Messenger; D012795:Sialoglycoproteins; D015675:Osteocalcin; D000469:Alkaline Phosphatase; D015232:Dinoprostone