2007 Fiscal Year Final Research Report Summary
The investigation for molecular mechanisms of aqueous humor outflow and the creation of new treatments for intraocular pressure elevation in glaucomatous eyes
| Project/Area Number |
18390470
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Ophthalmology
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| Research Institution | Kumamoto University |
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Principal Investigator |
TANIHARA Hidenobu Kumamoto University, Faculty of Medical and Pharmaceutical Sciences, Professor (60217148)
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| Co-Investigator(Kenkyū-buntansha) |
INATANI Masaru Kumamoto University, University Hospital, Lecturer (40335245)
KOGA Takahisa Kumamoto University, University Hospital, Lecturer (70372787)
ITO Yasuhiro Kumamoto University, University Hospital, Research associate (70380996)
KAWAJI Takahiro Kumamoto University, University Hospital, Research associate (30423677)
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| Project Period (FY) |
2006 – 2007
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| Keywords | glaucoma / aqueous humor outflow pathway / ROCK inhibitor / triamcinolone acetonide / amyloidosis |
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| Research Abstract |
The investigation for molecular mechanisms of aqueous humor outflow and the creation of new treatments for intraocular pressure elevation in glaucomatous eyes
The pathogenesis of primary open-angle glaucoma is derived from the unique optic neuropathy induced by intraocular pressure elevation. To treat the abnormal intraocular pressure elevation, we investigated for the resistance of aqueous humor outflow, a critical factor for intraocular pressure elevation. We examined pharmacological effects of ROCK inhibitors, which reduce aqueous humor resistance. Experiments using cultivated trabecular meshwork cells showed that ROCK inhibitor induces enhanced cell adhesion, relaxed cytoskeleton and changed structure of extracellular matrices. Moreover, our clinical trial for healthy volunteers showed that ROCK inhibitor dramatically reduces intraocular pressure in human eyes without serious side effects. The experiment using rabbit eyes showed that ROCK inhibitor keeps intraocular pressure lowering after the filtering surgery, a major glaucoma surgical procedure. Thus, we introduced ROCK inhibitors as new anti-glaucomatous drug, and inspired a new strategy for lowering intraocular pressure through physiological aqueous humor pathway. In addition, we examined the pathogenesis of secondary glaucoma, which is also induced by increased resistance of aqueous humor outflow. Triamcinolone acetonide, a popular corticosteroid drug, highly induces steroid-induced glaucoma. We reported the risk factors for steroid-induced glaucoma are the patients with young age, high baseline intraocular pressure, intravitreal injection of triamcinolone acetonide and high dose injection of triamcinolone acetonide. Last, we reported the complications after the surgery for a secondary glaucoma associated with familial amyloidosis, a hereditary disease exhibiting a high prevalence in Kumamoto, Japan.
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Research Products
(8 results)
