| Project/Area Number |
16390500
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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, Graduate School of Medical Sciences, Professor, 大学院・医学薬学研究部, 教授 (60217148)
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| Co-Investigator(Kenkyū-buntansha) |
FUKUSHIMA Mikiko Kumamoto University, Hospital, Associate Professor, 医学部附属病院, 講師 (10284770)
KOGA Takahisa Kumamoto University, Hospital, Associate Professor, 医学部附属病院, 講師 (70372787)
KOSHIYAMA Yasuo Kumamoto University, Graduate School of Medical Sciences, Assistant Professor, 大学院・医学薬学研究部, 助手 (40372784)
平田 憲 熊本大学, 医学部附属病院, 講師 (60295144)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥14,400,000 (Direct Cost: ¥14,400,000)
Fiscal Year 2005: ¥4,700,000 (Direct Cost: ¥4,700,000)
Fiscal Year 2004: ¥9,700,000 (Direct Cost: ¥9,700,000)
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| Keywords | ROCK / Rho / Glaucoma / Amyloidosis / Neuroprotection / Transthyretin / ROCK阻害薬 / ヒト培養線維柱帯細胞 / DNAマイクロアレイ / プロテオミクス |
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| Research Abstract |
We investigated molecular mechanisms of intraocular pressure elevation and optic nerve damage in glaucoma to develop new medical treatment for glaucoma. We showed the clinical results about surgical reconstruction for aqueous outflow to investigate aqueous outflow resistance (Arch Ophthalmol 2004). Then, we examined genetic analyses of glaucoma to identify the relationship between the genetics and the aqueous outflow resistance (Exp Cell Res 2004 ; IOVS 2004 ; J Glaucoma 2004 ; Mol Vis 2005). In addition, we elucidated the molecular mechanism of amyloid-induced secondary glaucoma, which is derived from a single gene mutation. We reported the localization of mutant transthyretin in ocular tissues, the difficulties in clinical treatments for the ocular complications and the possibility of the gene therapy (Transplantation 2004 ; Gene Therapy 2004 ; Amyloid 2004 ; Exp Eye Res 2005 ; Ophthalmology 2005). Moreover, we investigated the pharmacologic effect of ROCK inhibitor, which reduces the aqueous outflow resistance, for trabecular meshwork cells (Exp Eye Res 2006). On the other hand, we showed the pathological significance of the interaction between leukocytes and endothelium in eye diseases, and showed that the inhibition of the interaction induces the neuroprotective effect in retinal tissues (IOVS 2004 ; Arch Ophthalmol 2004 ; Pro Natl Acad Sci USA, 2003). We also showed that the eye in pathological conditions expresses bioactive factors, also resulting in neuroprotective effects (NeuroReport 2004), and that the stress response in endoplasmic reticula plays an important role in neuroprotection (J Neurochem 2006).
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