2017 Fiscal Year Final Research Report
Basic research for the pathogenesis of idiopathic epiretinal membranes
| Project/Area Number |
15K10910
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Ophthalmology
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| Research Institution | Osaka Medical College |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
奥 英弘 大阪医科大学, 医学部, 准教授 (90177163)
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| Co-Investigator(Renkei-kenkyūsha) |
Takai Shinji 大阪医科大学, 医学部, 教授 (80288703)
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| Research Collaborator |
Morishita Seita
Horie Taeko
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Keywords | 黄斑上膜 / 黄斑円孔 / セリンプロテアーゼ / トリプターゼ / キマーゼ / 抗２型コラーゲン抗体 / ニューステロイド / 免疫染色 |
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| Outline of Final Research Achievements |
To investigate the pathogenesis of idiopathic epiretinal membrane (ERM) from a biochemical perspective, the relationships between ERMs and tryptase activity and anti-type II collagen antibodies were investigated. Vitreous samples for measurement of tryptase activity were obtained from patients who underwent a vitrectomy for idiopathic macular hole (MH), proliferative diabetic retinopathy (PDR), ERM, and rhegmatogenous retinal detachment (RD). Anti-type II collagen antibodies were measured in serum obtained from the patients with ERM, PDR, and RD. Vitreal tryptase activity was significantly higher in MH and ERM than in PDR and RD. The serum levels of anti-type II collagen antibodies were significantly higher in the ERM and PDR than in RD. In the pathogenesis of ERM, increased vitreal tryptase activity may be involved in tissue fibrosis, and elevated serum anti-type II collagen antibodies may lead to an immune response at the vitreoretinal interface, thus resulting in membrane formation.
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| Free Research Field |
眼科学
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