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Morichika Takita
Department School of Medicine, School of Medicine Position Assistant Professor |
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| Article types | Original article |
| Language | English |
| Peer review | Peer reviewed |
| Title | Prostaglandin E receptor EP4 antagonist suppresses lipopolysaccharide-induced osteoclast formation and inflammatory bone loss. |
| Journal | Formal name：Journal of Health Science Abbreviation：J. Health Sci. ISSN code：13449702/13475207 |
| Domestic / Foregin | Domestic |
| Publisher | Pharmaceutical Society of JAPAN |
| Volume, Issue, Page | 53(2),pp.234-239 |
| Author and coauthor | Matsumoto Chiho†, Takita Moirichika, Inada Masaki, Maruyama Takayuki, Miyaura Chisato* |
| Authorship | 2nd author |
| Publication date | 2007/04 |
| Summary | PGE2 is mainly produced by osteoblasts in bone tissue, and acts as a potent stimulator of bone resorption. In osteoblasts, PGE2 production was greatly stimulated by lipopolysaccharide (LPS) following the expression of cyclooxygenase (COX)-2 and membrane-bound PGE synthase (mPGES)-1 mRNA. In the coculture of mouse bone marrow cells and osteoblasts, LPS induced PGE production and osteoclast formation, and EP4 antagonist completely suppressed osteoclast formation, indicating that PGE2-mediated EP4 signal is essential for LPS-induced osteoclast formation. Inflammatory bone diseases including periodontitis are known to be accompanied with the bone loss with increased osteoclastogenesis. To examine the role of EP4-medeiated PGE2 action in periodontitis, we examined the effects of EP4 antagonist on LPS-induced bone resorption using mouse alveolar bone. In organ culture of alveolar bone, LPS induced bone-resorbing activity and EP4 antagonist suppressed the LPS-induced bone resorption. In experimental model of periodontitis, LPS was injected into the lower gingiva and bone mineral density of alveolar bone was measured. LPS induced the loss of alveolar bone, which was recovered by the treatment of EP4 antagonist in vivo. Therefore, EP4 antagonist is a possible candidate for the therapy of inflammatory bone disease including periodontitis. |
| DOI | http://doi.org/10.1248/jhs.53.234 |