New treatment strategy for ocular fibrotic diseases by modulation of TGFbeta signal with TRP cation channnels

2016 Fiscal Year Final Research Report

• Project/Area Number: 25462729
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Ophthalmology
• Research Institution: Wakayama Medical University
• Principal Investigator: Saika Shizuya 和歌山県立医科大学, 医学部, 教授 (40254544)
• Project Period (FY): 2013-04-01 – 2017-03-31
• Keywords: 組織瘢痕化 / 成長因子 / TRPイオンチャネル / 角膜 / 眼 / ノックアウトマウス / 細胞培養 / 水晶体

Outline of Final Research Achievements

Tissue fibrosis induced by an alkali exposure was effectively suppressed by TRP channel (TRPA1, TRPV1, TRPV4)-signals modulation of TGFbeta-MAPK/Smad signals in genetically modified mouse lines. The inhibitory effects was reproduced by specific chemical inhibitors of each channel. TRPV4 signal was also found to be related to interleukin-6 signal in tissue fibrosis. A similar mechanism might be invilved in conjunctival fibrosis, although we have preliminary data. Tissue fibrosis in a mouse lens related to epithelial-mesenchymal transition did not seem to be related to TRP cation channel signals.

Free Research Field

眼科学