| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Research Abstract |
Bone destruction of rheumatoid arthritis (RA) is caused by abnormally activated osteoclasts. It is suggested that induction of heme oxygenase (HO)-1 is beneficial for the treatment of RA by reducing inflammation. The objective of this study is to clarify the influence of HO-1 and its repressor Bach1 on osteoclastogenesis and inflammatory bone loss. Through in vitro osteoclastogenesis experiments using bone marrow derived macrophages from Bach1 deficient mice, we demonstrate that down-regulation of HO-1 transcription, in which Bach1 as well as p38alpha is involved, is essential for the early stage of osteoclastogenesis. TNFalpha-induced inflammatory bone destruction and arthritis induced by collagen antibody are both reduced in Bach1 deficient mice. These findings support the hypothesis that up-regulation of HO-1 or inhibition of Bach1 activity represent promising therapeutic strategies for rheumatoid arthritis.
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