Development of new therapy for hemophilic arthropathy

• Project/Area Number: 26462286
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Orthopaedic surgery
• Research Institution: The University of Tokyo
• Principal Investigator: Hirose Jun 東京大学, 医学部附属病院, 講師 (00456112)
• Co-Investigator(Kenkyū-buntansha): 安井 哲郎 東京大学, 医学部附属病院, 講師 (30583108) ; 長村 登紀子 (井上登紀子 / 長村 登紀子(井上登紀子)) 東京大学, 医科学研究所, 准教授 (70240736) ; 竹谷 英之 東京大学, 医科学研究所, 講師 (90206996)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Project Status: Completed (Fiscal Year 2016)
• Budget Amount: ¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000); Fiscal Year 2016: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000); Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000); Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
• Keywords: 血友病性関節症 / 血友病 / モデルマウス / 血友病Bモデルマウス

Outline of Final Research Achievements

We made a hemophilic arthropathy model by inducing knee internal hemorrhage to hemophilia B model mice and analyzed them. We confirmed that joint destruction progressed with a time course by micro CT and histology. It was confirmed that TNFalpha, IL-1beta and IL-6 which were inflammatory cytokines increased by performing immunostaining. These results suggest that the increase of inflammatory cytokines is a potential cause of inflammation in hemophilic arthropathy. Osteoclasts were present in the synovium of the punctured knee and it was found that synovial cells expressed RANKL which is the factor indispensable for osteoclasts differentiation.