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2014 Fiscal Year Final Research Report

Identification of cells responsible for osteoclastogenesis in arthritis

Research Project

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Project/Area Number 25670636
Research Category

Grant-in-Aid for Challenging Exploratory Research

Allocation TypeMulti-year Fund
Research Field Orthopaedic surgery
Research InstitutionThe University of Tokyo

Principal Investigator

TAKAYANAGI Hiroshi  東京大学, 医学(系)研究科(研究院), 教授 (20334229)

Project Period (FY) 2013-04-01 – 2015-03-31
Keywords破骨細胞
Outline of Final Research Achievements

In order to functionally demonstrate in vivo which cell types drive pathogenic osteoclast differentiation we used Tnfsf11a floxed mice for the depletion of RANKL in T-cells and synovial fibroblasts during collagen antibody-induced arthritis (CAIA). The accurate assessment of the osteoclast erosions was performed by micro-CT analysis. Significant increases in osteoclast numbers and bone erosions were observed in the Tnfsf11flox/Δ Lck-Cre and Tnfsf11flox/Δ Col2a1-Cre groups during CAIA, however, the Tnfsf11flox/Δ Col6a1-Cre mice showed significant protection against osteoclast formation and bone erosions. Thus, it is suggested that RANKL expression by synovial fibroblasts rather than T-cells govern the osteoclast differentiation that leads to inflammation-associated joint destruction.

Free Research Field

骨免疫学

URL: 

Published: 2016-06-03  

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