Plectin and PPP1r18 regulate RANKL production of osteocytes by mechanical stress

2021 Fiscal Year Final Research Report

• Project/Area Number: 19K19257
• Research Category: Grant-in-Aid for Early-Career Scientists
• Allocation Type: Multi-year Fund
• Review Section: Basic Section 57070:Developmental dentistry-related
• Research Institution: Tohoku University
• Principal Investigator: Maeda Toshihiro 東北大学, 歯学研究科, 大学院非常勤講師 (50792149)
• Project Period (FY): 2019-04-01 – 2022-03-31
• Keywords: 骨細胞 / 機械的刺激 / RANKL / PPP1r18 / Plectin

Outline of Final Research Achievements

Using our established live imaging experimental system, it was clarified that actin remodeling and changes in cell morphology occur in calcium response-positive cells that sense mechanical stress. In addition, by using this mechanical loading device, the expression of RANKL mRNA and protein in primary osteocytes was increased by mechanical stress. Furthermore, co-culture experiments with mechanically stimulated primary osteocytes and osteoclast progenitor cells revealed that osteoclast differentiation was promoted in the mechanically stimulated group. It was confirmed that mechanical stress affects the expression of plectin and PPP1r18 in osteocytes.

Free Research Field

歯科矯正学

Academic Significance and Societal Importance of the Research Achievements

本研究では、機械的刺激による骨細胞におけるRANKL 発現増加の分子メカニズム解明のため、これまで骨細胞における発現と機能が未知なplectin と PPP1r18 に着目し解明を行う点に独自性がある。本研究により、骨細胞のmechanotransduction メカニズムの解明につながることが期待される。
本研究による機械的刺激が促す破骨細胞分化の分子メカニズムの解明は、健常者だけでなく、大理石骨病や骨粗しょう症への薬物療法など、歯の動きが遅延することが知られる症例における矯正歯科治療の効率化にもつながり、本研究は臨床応用への展開が期待される基礎研究として、大きな意義を持つ。