(18-10-07) PGE2 Activates Cementoclastogenesis by Cementoblasts via EP4.

Oka H, Miyauchi M, Sakamoto K, Moriwaki S, Niida S, Noguchi K, Somerman MJ, Takata T.
Department of Oral and Maxillofacial Pathobiology, Graduate School of Biomedical Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8553, Japan;
Destruction of cementum and alveolar bone is the main causative event for the exfoliation of teeth as a consequence of periodontitis. Prostaglandin E(2) (PGE(2)) and PGE receptor subtypes (EPs) play an important role in modulating osteoblast-mediated osteoclastogenesis; however, no information is available on the role of PGE(2) and EPs in regulating cementoblast-mediated cementoclastogenesis. We hypothesized that the PGE(2)-EPs pathway also regulates cementoblasts' ability to activate cementoclasts. For these studies, OCCM-30 cells (a mouse cementoblast cell line) were exposed to PGE(2) and specific EP agonists. PGE(2) (100 ng/mL) and EP4 agonist (1 muM) up-regulated RANKL and IL-6 mRNA levels, while they down-regulated OPG mRNA expression. The EP4 antagonist (1 muM) eliminated these effects of PGE(2). PGE(2) treatment of co-cultures of OCCM-30 cells with bone marrow cells induced TRAP-positive cells via the EP4 pathway. These findings suggest that PGE(2) promotes cementoblast-mediated cementoclastogenesis by regulating the expression of RANKL and OPG via the EP4 pathway.

Fonte: J Dent Res

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