Involvement of FGF-2 in the action of Emdogain on normal human osteoblastic activity.
OBJECTIVE
The present study was designed to evaluate the pharmacological characteristics of Emdogain (EMD) on cell growth and cell activity in human osteoblasts.


METHODS
Cell proliferation as well as several gene and protein expressions were examined using reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA) procedures in human osteoblastic cells (SaM-1) treated with EMD (30 microg ml(-1)).


RESULTS
Treatment of osteoblasts with EMD significantly stimulated cell proliferation and fibroblast growth factor (FGF)-2 expression but decreased alkaline phosphatase expression. In addition, increases in cyclooxygenase (COX)-2 expression and decreases in matrix metalloproteinases (MMP)-1 expression were observed in osteoblasts treated with EMD. The effects of EMD on FGF-2 and MMP-1 expressions were not observed in osteoblasts treated with NS-398, an inhibitor of COX-2. The decrease in MMP-1 mRNA by EMD was prevented by treatment with antisense oligodeoxynucleotide (AS-ODN) for FGF-2.


CONCLUSIONS
Emdogain showing both stimulation of cell proliferation and inhibition of cell differentiation has been shown to increase FGF-2 expression in the mediation of prostaglandin E2 and to decrease MMP-1 mRNA expression through the activation of FGF-2. FGF-2 may underlie in the action of EMD on osteoblasts during periodontal regeneration.
Mizutani
S
S
Department of Pharmacology, School of Dentistry, Aichi-Gakuin University, Nagoya, Japan.
Tsuboi
T
T
Tazoe
M
M
Koshihara
Y
Y
Goto
S
S
Togari
A
A
D000328:Adult; D000469:Alkaline Phosphatase / Q000187:drug effects; D002454:Cell Differentiation / Q000187:drug effects; D002455:Cell Division / Q000187:drug effects; D002478:Cells, Cultured; D051546:Cyclooxygenase 2; D052246:Cyclooxygenase 2 Inhibitors; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D016373:DNA, Antisense / Q000494:pharmacology; D003746:Dental Enamel Proteins / Q000494:pharmacology*; D016222:Fibroblast Growth Factor 2 / Q000187:drug effects* / Q000235:genetics; D005786:Gene Expression Regulation / Q000187:drug effects; D015971:Gene Expression Regulation, Enzymologic / Q000187:drug effects; D006801:Humans; D007527:Isoenzymes / Q000037:antagonists & inhibitors / Q000187:drug effects; D008297:Male; D020781:Matrix Metalloproteinase 1 / Q000187:drug effects; D008565:Membrane Proteins; D009578:Nitrobenzenes / Q000494:pharmacology; D010006:Osteoblasts / Q000187:drug effects*; D010544:Peroxidases / Q000037:antagonists & inhibitors / Q000187:drug effects; D011451:Prostaglandin-Endoperoxide Synthases / Q000187:drug effects; D013449:Sulfonamides / Q000494:pharmacology
D052246:Cyclooxygenase 2 Inhibitors; D016861:Cyclooxygenase Inhibitors; D016373:DNA, Antisense; D003746:Dental Enamel Proteins; D007527:Isoenzymes; D008565:Membrane Proteins; D009578:Nitrobenzenes; D013449:Sulfonamides; C109069:enamel matrix proteins; D016222:Fibroblast Growth Factor 2; C080955:N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide; D010544:Peroxidases; D051546:Cyclooxygenase 2; C496540:PTGS2 protein, human; D011451:Prostaglandin-Endoperoxide Synthases; D000469:Alkaline Phosphatase; D020781:Matrix Metalloproteinase 1