The mechanism of corneal ulcer and corneal fibrosis mediated by alarmin signaling pathway
| Project/Area Number |
26861453
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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 | Yamaguchi University |
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Principal Investigator |
ORITA Tomoko 山口大学, 医学(系)研究科(研究院), 助教 (50467792)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 角膜性角膜腫瘍 / 自然免疫 / コラーゲン分解 / アラーミン分子 / 角膜線維芽細胞 / 感染性角膜腫瘍 / 感染性角膜潰瘍 |
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| Outline of Final Research Achievements |
Alarmins were obtained as the materials released from HCE and HKC cells after freezing and thawing. The alamins contained mainly IL-1α, HMGB-1. They activated NF-κB and MAPK signaling pathway. Next we examined the hydroxyproline assay and the expression of MMP-2, 3 and 9. The alarmins induced hydroxyproline and the expression of MMP-2, 3, 9 as well. This indicates the alarmins promoted collagen degradation. Finally we evaluated the effects of alramins to the barrier function in HCE. The alramins reduced TER and inhibited the expression of ZO-1, occluding, E-cadherin and β-catenin. This indicates that the alarmins may involve in barrier dysfunction in HCE cells.
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Report
(3 results)
Research Products
(26 results)
