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

2017 Fiscal Year Final Research Report

• 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
• 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

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.

Free Research Field

形成外科学