Inhibitory mechanism of caldecrin on RANKL-stimulated signaling platform formation in the osteoclasts

2014 Fiscal Year Final Research Report

• Project/Area Number: 24592811
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Functional basic dentistry
• Research Institution: Meikai University
• Principal Investigator: TOMOMURA Akito 明海大学, 歯学部, 教授 (60188810)
• Co-Investigator(Kenkyū-buntansha): TOMOMURA Mineko 明海大学, 歯学部, 准教授 (30217559)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: カルシウム / 破骨細胞 / 分化 / プロテアーゼ / ラフト

Outline of Final Research Achievements

Inhibitory mechanism of serum calcium-decreasing factor, caldecrin, on the osteoclastogenesis was investigated. RANKL activates raft-independent signaling pathways (NFκB, ERK and JNK), and raft-dependent signaling pathway (Fyn, Syk and PLCγ) in the RAW264.7 cells. Caldecrin inhibited only the raft-dependent signaling pathway. The phosphorylation of Fyn on the raft domain of plasma membrane was increased by RANKL but not in the presence of caldecrin. Disruption of raft domain impaired the RANKL-stimulated and caldecrin-inhibited phosphorylation of Fyn. These results suggest that caldecrin inhibits the osteoclastogenesis by the inhibition of the RANKL-stimulated activation of Fyn on the signal platform on the plasma membrane.

Free Research Field

生化学、分子生物学、骨代謝学