New treatment strategy for ocular fibrotic diseases by modulation of TGFbeta signal with TRP cation channnels
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)
|
Co-Investigator(Kenkyū-buntansha) |
住岡 孝吉 和歌山県立医科大学, 医学部, 講師 (40433362)
山中 修 和歌山県立医科大学, 医学部, 博士研究員 (50254545)
岡田 由香 和歌山県立医科大学, 医学部, 准教授 (50264891)
|
Project Period (FY) |
2013-04-01 – 2017-03-31
|
Project Status |
Completed (Fiscal Year 2016)
|
Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
|
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 / TRPV4 / TRPA1 / イオンチャンネル / 創傷治癒 / 線維化 / シグナル / TRPチャネル / TGFβシグナル / Smad / MAPキナーゼ / 線維芽細胞 / 炎症 / 瘢痕 |
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.
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Report
(5 results)
Research Products
(36 results)