Study on inhibitory effects of synthetic Peptide derived from TRAF1 on osteoclast differentiation

2014 Fiscal Year Final Research Report

• Project/Area Number: 24390437
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: Prosthetic dentistry
• Research Institution: Kyushu University
• Principal Investigator: MAKIHIRA Seicho 九州大学, 歯学研究科(研究院), 准教授 (80304450)
• Co-Investigator(Kenkyū-buntansha): SHINOHARA Yoshinori 九州大学, 大学院歯学研究院, 助教 (00423533) ; HATSUMI Nagadome 九州大学, 大学院歯学研究院, 助教 (30284516) ; MASAKI Honda 日本大学, 歯学部, 准教授 (70361623)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: TRAF1 / 骨吸収 / ペプチド / 破骨細胞 / 膜通過

Outline of Final Research Achievements

There is a need for the development of a material with few side effects to treat diseases of osteolysis, such as a bisphosphonate-related osteonecrosis of the jaw. We previously showed that TRAF1, a member of the TRAF family, is a negative regulator of RANKL-dependent osteoclastogenesis. We thus hypothesized that synthetic peptides derived from TRAF1 could have a similar function in pre-osteoclast cells. Two peptides derived from TRAF1 (T1 and T2), N-terminally conjugated with an eleven-arginine sequence (11R), were synthesized. 11R is well known as a membrane-permeable sequence.T1 decreased the number of TRAP-positive osteoclasts in RAW264.7 cells stimulated with RANKL compared to those in RANKL- stimulated cells without T1. On the other hand, 11R and T2 had no effect on these in RAW264.7 exposed to RAW264.7RANKL.The results suggest that a synthetic peptide derived from TRAF1 may be a candidate of therapeutic agent to block osteolysis.

Free Research Field

歯科補綴学