The establishment of thrapeticstrategy based on corneal stroma melting mechanism in severe cases of neurokeratopaty

2021 Fiscal Year Final Research Report

• Project/Area Number: 19K09937
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Review Section: Basic Section 56060:Ophthalmology-related
• Research Institution: Wakayama Medical University
• Principal Investigator: Okada Yuka 和歌山県立医科大学, 医学部, 教授 (50264891)
• Co-Investigator(Kenkyū-buntansha): 雑賀 司珠也 和歌山県立医科大学, 医学部, 教授 (40254544) ; 住岡 孝吉 和歌山県立医科大学, 医学部, 准教授 (40433362)
• Project Period (FY): 2019-04-01 – 2022-03-31
• Keywords: 神経麻痺性角膜症 / マウスモデル

Outline of Final Research Achievements

To understand pathobiology of neurotrophic keratopathy we established a severe mouse model of neurotrophic keratopathy by coagulating(18G) the first branch of the trigeminal nerve (V1 nerve).
The corneal opacity and inflammation appeared from an early stage (6 hours later) in the severe model. When observed until 2 years, invasion of inflammatory cells into the corneal stroma was observed for a long period of time, and the corneal stroma was thinner. The corneal epithelium was layered and thickened. This phenomenon may be compensating for the storomal thinning. Since the immunostaining property of keratin 12 (specific keratin of the corneal epithelium) had disappeared, the corneal epithelium was replaced with the conjunctival epithelium instead of the corneal epithelium, and staining of involucrin, which is a marker of keratinization, was observed.

Free Research Field

眼科

Academic Significance and Societal Importance of the Research Achievements

神経麻痺性角膜症は難治性疾患で、現在対症療法しかない。重症モデルの詳細な組織病理学的検討とその発症メカニズムは重要な課題であるものの、十分な検討が行われていなかったため、重症神経麻痺性角膜症について検討を行う必要がある。
マウスモデルを作成し、病態を解明することで、難治性で、対症療法しか行えなかった神経麻痺性角膜症の病態ターゲットを標的とした治療に繋がると考えている。