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J.Health Sci., 55(3), 389-395, 2009
Prostaglandin E2 Increases the Expression of B-Type Natriuretic Peptide Receptor through EP1 Receptor, Ca2+ Mobilization and Protein Kinase C Signaling Pathway in Rat Calvarial Osteoblasts
Hiroyuki Kaneki,*, a Maki Kurokawa-Nagai,a
Yuri Sugano,a Gaku Ishi-i,a
Minoru Kurokawa,band Hayao Ideaa
aFaculty of Pharmaceutical Sciences, Toho University, 2-2-1 Miyama, Funabashi, Chiba 274-8510, Japan and
bDepartment of Pharmacy, University of Toho Medical Center, Omori Hospital, 6-11-1 Omori-Nishi, Ota-ku, Tokyo 143-8541, Japan
The C-type natriuretic peptide stimulates osteoblastic functions through the B-type natriuretic receptor (NPR-B). In this study, we examined the signaling pathway behind the regulation of NPR-B expression through the prostaglandin E2 (PGE2) receptor, EP1 subtype using rat calvarial osteoblasts. A23187 as a Ca2+ ionophore increased NPR-B expression dose-dependently. PGE2 or 17-phenyl-ω-trinor PGE2 (EP1A), an EP1 agonist, increased NPR-B expression, and the potentiating effects were blocked by treating with BAPTA-AM as an intracellular Ca2+ chelator. Activators of protein kinase C (PKC), 1-oleoyl-2-acetyl-sn-glycerol, a membrane-permeable diacylglycerol, and 12-o-tetradecanoyl-phorbol-13-acetate, also increased NPR-B expression, and the potentiating effects were blocked by treating with BAPTA-AM. The treatment of cells with GF109203X, a PKC inhibitor, blocked the PGE2- and EP1A-induced increase in NPR-B expression. From these results, we concluded that EP1-mediated increase in the expression of NPR-B requires not only Ca2+ mobilization but also PKC activation through the activation of phosphatidylinositol-specific phospholipase C.
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