Investigation of regulatory mechanisms of aqueous outflow based on molecular signalings of TGF-beta and proinflammatory cytokines.
| Project/Area Number |
25861640
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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 |
Ophthalmology
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| Research Institution | Kumamoto University |
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Principal Investigator |
INOUE MIYUKI 熊本大学, 大学院生命科学研究部(医), 特任助教 (20631766)
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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 |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 緑内障 / 線維柱帯細胞 / TGF-β2 / サイトカイン |
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| Outline of Final Research Achievements |
To investigate the regulatory mechanisms of aqueous outflow, we assessed the cross talk between TGF-β2 and proinflammatory cytokines in human trabecular meshwork cells, because those levels in aqueous humor were elevated in glaucoma patients. We examined the effect of TGF-β2 on the expression of extracellular matrix. TGF-β2 induced the production of type I collagen, and the effect was significantly inhibited by p38 inhibitor but not by ROCK inhibitor. Additionally, we found that TGF-β2 induced the production of IL-6 and IL-8 from trabecular meshwork cells. Furthermore, TGF-β2 increased the expression of alpha-SMA, and the induction was inhibited by treatment with IL-6 in a dose-dependent manner. These data suggest that the crosstalk between TGF-β2 and cytokine signalings may relate to the regulation of aqueous outflow. We are going to examine the molecular mechanisms of this cross talk between TGF-β2 and proinflammatory cytokines more closely in human trabecular meshwork cells.
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Report
(3 results)
Research Products
(6 results)
