| Project/Area Number |
15K15638
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Ophthalmology
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| Research Institution | Kyoto Prefectural University of Medicine |
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Principal Investigator |
Hamuro Junji 京都府立医科大学, 医学(系)研究科(研究院), 特任教授 (80536095)
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| Research Collaborator |
YAMAWAKI TAKAHIRO
ITO EIKO
MUKAI ATSUSHI
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | エキソゾーム / 網膜色素上皮細胞 / マクロファージ / 補体活性化抑制因子 / 加齢黄斑変性症 / miRNA / マクロフアージ / 補体系関連因子 / 細胞外微粒子 / 加齢黄斑変性 / 補体系活性化抑制因子 / 炎症増悪回路 |
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| Outline of Final Research Achievements |
The new approach to develop the pioneering pharmaceuticals to prevent the progression of AMD pathogeneis were proposed. The degenerated RPE are turned out to lose the phｙsiological homeostatic regulatory activities such as to contorol the overactivation of alternative pathway of complement activation by the decreased production of complement activation inhibitory factors and the loss of the inhibition of proinflammatory TNFa by Mps.
These berakdown of phisiological functions of RPE is mainly due to the interaction with Mps infiltrated into subretina. The EVs, detected as CD63 positive microvesicles released from RPE was strikingly incerased when RPE was cocultured with Mps and thease EVs mediated some of the dysfunctions of RPE in subretinal microenvironments.The interactions were analysed both in murine and human co-culture systems.Thease findings may suggest the new molecular target for the design of th durg for AMD.
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