The mechanism of corneal ulcer and corneal fibrosis mediated by alarmin signaling pathway

2015 Fiscal Year Final Research Report

• Project/Area Number: 26861453
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Ophthalmology
• Research Institution: Yamaguchi University
• Principal Investigator: ORITA Tomoko 山口大学, 医学(系)研究科(研究院), 助教 (50467792)
• Project Period (FY): 2014-04-01 – 2016-03-31
• 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

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.

Free Research Field

医歯薬学