Investigation of glaucoma pathology focusing on epigenome and fibrocyte in aqueous humor dynamics and wound healing

2019 Fiscal Year Final Research Report

• Project/Area Number: 17H04351
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Ophthalmology
• Research Institution: Kumamoto University
• Principal Investigator: TANIHARA Hidenobu 熊本大学, 病院, 病院長 (60217148)
• Co-Investigator(Kenkyū-buntansha): 井上 俊洋 熊本大学, 大学院生命科学研究部(医), 教授 (00317025) ; 藤本 智和 熊本大学, 大学院生命科学研究部(医), 助教 (50756426) ; 高橋 枝里 熊本大学, 病院, 講師 (60622602)
• Project Period (FY): 2017-04-01 – 2020-03-31
• Keywords: 緑内障 / エピゲノム / 線維柱帯 / 結膜線維芽細胞

Outline of Final Research Achievements

Our purpose of this study was the involvement of epigenome in glaucoma pathology, and drug discovery by identifying new targets. The HDAC inhibitor vorinostat was evaluated for the conventional outflow, and it was revealed that it significantly suppressed the increase in outflow resistance induced by TGF-β2. In addition, the effect of conjunctival scarring on the prognosis of glaucoma filtration surgery was evaluated using conjunctival fibroblasts. Both vorinostat and decitabine were found to have the effect of suppressing the transformation of conjunctival fibroblasts into myofibroblasts by TGF-β2. These results indicate that epigenetic drugs may be effective in treating glaucoma.

Free Research Field

眼科学

Academic Significance and Societal Importance of the Research Achievements

本研究によって、緑内障進行に影響を与える眼圧調節に対してエピゲノムの関与が示され、眼圧下降剤としてのHDAC阻害剤の可能性も示された。また、緑内障濾過手術後の眼圧調節において濾過胞の維持が重要であるが、エピジェネティクス薬が瘢痕化を抑制する可能性を示したことから術後予後を改善する治療薬としての可能性も考えられる。