| Project/Area Number |
25860571
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Gastroenterology
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| Research Institution | Fukuoka University |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 消化管リモデリング / 線維化・癌化 / 線維芽細胞 / カルシウム / TRPC6 / 細胞外マトリックス / ストレスファイバー / myofibroblast / intestine / Ca2+ / TGF-β / fibrosis / tumor microenvironment / stress / 大腸癌 / 癌関連線維芽細胞 / 癌微小環境 / チロシンリン酸化 / 成長因子 |
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| Outline of Final Research Achievements |
The crucial role of intestinal fibroblasts/myofibroblasts in inflammation, fibrosis, cancer microenvironment formation is well established. Available evidence suggests that part of fibroblasts/myofibroblasts function may reflect altered Ca2+ homeostasis. We focused TRPC6 function in growth factors-mediated signaling associated with tissue remodeling. Our data suggested that myofibroblast TRPC6 channel modulating stress fiber formation, cell-cell adhesion, extracellular matrix synthesis, and cytokine secretion. Growth factors-mediated signaling in intestinal myofibroblasts comprises several phosphorylation events, and forms an intricate network involving TRPC6-mediated signaling pathways. These results suggest that TRPC6-associated myofibroblastic differentiation could be an important process promoting intestinal remodeling, and thus a promising target for future anti-fibrotic and anti-tumorgenesis therapies in the gut.
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