Analysis of mechanotransduction system in neurofibromatosis type I and application to the treatment of abnormal scars

Research Project

Project/Area Number	16K15750
Research Category	Grant-in-Aid for Challenging Exploratory Research
Allocation Type	Multi-year Fund
Research Field	Plastic surgery
Research Institution	Osaka University
Principal Investigator	KUBO Tateki 大阪大学, 医学系研究科, 准教授 (00362707)
Project Period (FY)	2016-04-01 – 2018-03-31
Project Status	Completed (Fiscal Year 2017)
Budget Amount *help	¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000) Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000) Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Keywords	レックリングハウゼン病 / RhoA / Neurofibromin / 筋線維芽細胞 / 機械的伸展刺激 / neurofibromin / 創傷治癒
Outline of Final Research Achievements	Our findings have suggested that neurofibromin was involved in the differentiation of fibroblasts to myofibroblasts in response to mechanical stimulation. When neurofibromin was dysfunctional or suppressed, the unresponsiveness to mechanical stimulation in the actin polymerization occurred, which might lead to the unchanging expression of α-SMA. Furthermore, actin stabilizer also did not promote α-SMA expression in normal HDFs in response to mechanical stimulation. We believe that this molecular pathway can be a potential therapeutic target to treat abnormal scars.