Experimental study on elucidation of target molecule of joint contracture and development of therapeutic strategy for new physical therapy

2017 Fiscal Year Final Research Report

• Project/Area Number: 15H03045
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Rehabilitation science/Welfare engineering
• Research Institution: Nagasaki University
• Principal Investigator: OKITA Minoru 長崎大学, 医歯薬学総合研究科(保健学科), 教授 (50244091)
• Co-Investigator(Kenkyū-buntansha): 中野 治郎 長崎大学, 医歯薬学総合研究科(保健学科), 准教授 (20380834) ; 坂本 淳哉 長崎大学, 医歯薬学総合研究科(保健学科), 准教授 (20584080) ; 本田 祐一郎 長崎大学, 病院(医学系), 技術職員 (40736344) ; 佐々部 陵 長崎大学, 病院(医学系), 技術職員 (50710985)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: 拘縮 / 関節包 / 靱帯 / 線維化 / 標的分子 / HIF-1α / 理学療法 / 治療戦略

Outline of Final Research Achievements

In this study, we used an experimental animal model of joint contracture to investigate the molecular mechanisms of the contracture derived from changes in joint capsule and ligament. As a result, the fibrosis of the joint capsule, which is the main pathology of contracture, is a change caused by the increase of type I collagen, suggesting that the producing cell is myofibroblast. On the other hand, in the ligament, fibrosis was not observed, and collagen production was decreased. Therefore, we guessed that the ligament did not contribute to the responsible lesion of contracture. In addition, intervention experiments were conducted to induce cyclic muscle contraction in the skeletal muscle during the progress of contracture and to promote muscle pumping action. As a result, expression of HIF-1α assumed to be a target molecule of contracture was suppressed, and it became clear that occurrence of fibrosis can also be prevented.

Free Research Field

リハビリテーション科学