• Search Research Projects
  • Search Researchers
  • How to Use
  1. Back to project page

2018 Fiscal Year Final Research Report

Molecular mechanism of bone destruction in rheumatoid arthritis based on CD147

Research Project

  • PDF
Project/Area Number 16K08567
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field General pharmacology
Research InstitutionNagasaki International University

Principal Investigator

NISHIOKU TSUYOSHI  長崎国際大学, 薬学部, 准教授 (90435115)

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)
Project Period (FY) 2016-04-01 – 2019-03-31
KeywordsCD147 / ポドソーム / 破骨細胞
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.

Free Research Field

骨代謝

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。

URL: 

Published: 2020-03-30  

Information User Guide FAQ News Terms of Use Attribution of KAKENHI

Powered by NII kakenhi