| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| 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.
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