| Project/Area Number |
16K08567
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
General pharmacology
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| Research Institution | Nagasaki International University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
岡元 邦彰 岡山大学, 医歯薬学総合研究科, 教授 (10311846)
筑波 隆幸 長崎大学, 医歯薬学総合研究科(歯学系), 教授 (30264055)
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | CD147 / ポドソーム / 破骨細胞 / 薬理学 |
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| Outline of Final Research Achievements |
We examined the hypothesis that CD147, which is upregulated in rheumatoid arthritis, enhances actin ring formation via podosome. In osteoclastogenisis, CD147 expression was significantly increased and localized to the cell membrane. We confirmed podosome marker expression and actin ring formation in osteoclasts, and CD147 co-localized with actin ring. We examined the expression of MT1-MMP, which is involved in the sealing by actin ring, and increased expression was observed in osteoclasts. However, the interaction between CD147 and MT1-MMT could not be confirmed. It has been shown that CD147, which is upregulated in osteoclasts, may be involved in podosome formation.
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| Academic Significance and Societal Importance of the Research Achievements |
生物学的製剤はその優れた有効性の反面、安全性や投与経路の問題ならびに高額な治療費のため寛解導入率は3割にすぎない。また、薬物治療の効果が十分に得られない患者も存在しており、経口投与可能かつ安価で安全性の高い新規抗リウマチ薬の開発が重要課題となっている。破骨細胞のポドソーム形成におけるCD147の分子機構をより詳細に解明し、CD147を標的とした新規抗リウマチ薬の創薬基盤の提示、関節リウマチの治療法構築の活路を開くことが可能である。本研究成果ならびに研究の継続による生物学的製剤と同等の有効性かつ安価な新規抗リウマチ薬の開発は、骨破壊の抑制を可能とし、患者のADL障害を防御することが可能である。
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