| Project/Area Number |
15K10872
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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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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| Co-Investigator(Kenkyū-buntansha) |
井上 俊洋 熊本大学, 医学部附属病院, 講師 (00317025)
谷原 秀信 熊本大学, 大学院生命科学研究部(医), 教授 (60217148)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 緑内障 / 線維柱帯細胞 / TGF-β2 / IL-6 / soluble IL-6 receptor / 可溶性IL-6レセプター / STAT3 |
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| Outline of Final Research Achievements |
To investigate the regulatory mechanisms of aqueous outflow, we assesed the crosstalk 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 and IL-6 signals on the expression of actin polymerization,α-SMA and TGF-βsignals.We confirmed IL-6 production induced by TGF-β2 in HTM cells, and production of IL-6 and soluble IL-6 receptor in aqueous outflow of glaucoma patients.We examined that the crosstalk between TGF-β and IL-6 signals may relate to the regulation of aqueous outflow. TGF-β2 induced actin polymerization,α-SMA production and activation of TGF-β2 signals. However,these effects were inhibited by treatment with IL-6/sIL-6R.Furthermore,knockdown of STAT3 is downstream of IL-6 signals inhibited the effects. These data suggests that the crosstalk between TGF-β2 and IL-6/sIL-6R signals may relate to the regulation of aqueous outflow.
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