| Project/Area Number |
25861319
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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 |
Orthopaedic surgery
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| Research Institution | Okayama University |
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Principal Investigator |
Kawabata Tomoko 岡山大学, 医歯(薬)学総合研究科, 助教 (90600669)
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| Research Collaborator |
OGAWA Hiroko 岡山大学, 医歯薬学総合研究科 地域医療人材育成講座, 助教
NISHIDA Keiichiro 岡山大学, 医歯薬学総合研究科 機能再生・再建科学講座 人体構成学分野, 准教授
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | MDM2 / HDAC1 / 関節リウマチ / TNFα / アポトーシス / ＭＤＭ２ / ＨＤＡＣ1 / ｐ53 / ＭＤＭ２阻害剤 / p53 |
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| Outline of Final Research Achievements |
Rheumatoid arthritis (RA) is an autoimmune disease characterized by chronic inflammation of the synovial tissues in multiple joints that leads to bone and joint destruction. Recent clinical application of biologic agents targeted to inflammatory cytokines including tumor necrosis factor α (TNFα) or interleukin-1β (IL)-1β dramatically changed the treatment strategy for RA. Nevertheless, the etiology of RA inflammation still remains unknown, and there is a demand for developing new therapies with alternative targets. We reported that expression of HDAC1 were significantly higher in RA than in OA synovial tissues, and they were upregulated by TNFα stimulation in RASFs. Previos report indicated that Mdm2-HDAC1 complex deacetylates p53. Our result showed that the protein level of nuclear p53 was higher in RASF which treated MDM2 inhibitor and apoptosis of RASF was induced in TUNEL staining. MDM2 inhibitor may induce cell cycle arrest and/or apoptosis as new RA therapies.
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