2013 Fiscal Year Final Research Report
Research into the role of HO-1 and its repressor Bach1 on osteoclastogenesis
| Project/Area Number |
24791001
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
膠原病・アレルギー・感染症内科学
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| Research Institution | Yokohama City University |
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Principal Investigator |
HAMA Maasa 横浜市立大学, 附属病院, 助教 (70574169)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Keywords | 関節リウマチ / 破骨細胞 / HO-1 / Bach1 |
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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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Research Products
(4 results)
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[Journal Article] Bach1 regulates osteoclastogenesis via both heme oxygenase-1 dependent and independent pathways2012
Author(s)
Hama M, Kirino Y, Takeno M, Takase K, Miyazaki T, Yoshimi R, Ueda A, Itoh-Nakadai A, Muto A, Igarashi K, Ishigatsubo Y
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Journal Title
Arthritis Rheum
Volume: 64(5)
Pages: 1518-28
Peer Reviewed
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