• Search Research Projects
  • Search Researchers
  • How to Use
  1. Back to project page

2014 Fiscal Year Final Research Report

Novel mechanism of regulating the activity of the transcription factor NFATc1 in bone metabolism

Research Project

  • PDF
Project/Area Number 24592821
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Functional basic dentistry
Research InstitutionMatsumoto Dental University

Principal Investigator

YAMASHITA Teruhito  松本歯科大学, 総合歯科医学研究所, 准教授 (90302893)

Co-Investigator(Kenkyū-buntansha) NINOMIYA Tadashi  松本歯科大学, 総合歯科医学研究所, 講師 (00360222)
TAKAHASHI Naoyuki  松本歯科大学, 総合歯科医学研究所, 教授 (90119222)
Research Collaborator KADOTA Shigetoshi  
KIKUCHI Takanobu  
Project Period (FY) 2012-04-01 – 2015-03-31
Keywords破骨細胞 / 転写因子 / NFATc1 / リン酸化
Outline of Final Research Achievements

Arctigenin was previously shown to inhibit osteoclastogenesis; however, this inhibitory mechanism has yet to be elucidated. In this study, we showed that arctigenin inhibited the action of NFATc1 by novel mechanism. Arctigenin strongly inhibited RANKL-induced osteoclast formation in mouse bone marrow macrophage (BMM) cultures, in which the calcineurin-dependent NFATc1 pathway was activated. Arctigenin, but not cyclosporin A suppressed osteoclast formation in co-cultures of osteoblastic cells and bone marrow cells, in which the osteoblastic cell-dependent NFATc1 pathway was activated. ChIP analysis confirmed that arctigenin inhibited the recruitment of NFATc1 to the promoter region of the NFATc1 target gene. These results suggest that arctigenin induces a dominant negative species of NFATc1, which inhibits osteoclast differentiation and function by suppressing both calcineurin-dependent and osteoblastic cell-dependent NFATc1 pathways.

Free Research Field

口腔生化学

URL: 

Published: 2016-06-03  

Information User Guide FAQ News Terms of Use Attribution of KAKENHI

Powered by NII kakenhi