Research for associations of tension-dependent aqueous outflow regulation by trabecular meshwork with glaucoma pathology.
| Project/Area Number |
21791693
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Ophthalmology
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| Research Institution | Kumamoto University |
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Principal Investigator |
INOUE Toshihiro Kumamoto University, 大学院・生命科学研究部, 助教 (00317025)
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2010: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2009: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 眼科 / 緑内障 / 房水流出路 / 眼圧 / 線維柱帯 / 圧感受性 / アクチン / 房水流出率 / 3次元培養 |
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| Research Abstract |
To identify factors associated with the tension-dependency, we developed a pressure model by using three-dimension culture of trabecular meshwork cells. In this model, collagen, medium, and cells were mixed and then were stabilized by changing the pH. After letting cells migrate and proliferate in the model, the model was weighed, and cells in the model were observed by immunostaining. F-actin was found to be decreased by observation with the confocal microscopy. Considering ROCK inhibitors which decrease F-actin could lower intraocular pressure in human, we assumed that this response contributed to the homeostasis of intraocular pressure by using the same mechanism with ROCK inhibitors. It was difficult, however, to approach proteins in cells in the three-dimension culture. We therefore assessed the reaction of trabecular cells against oxidative stress, because we speculated that the intracellular reaction against pressure stress had similar aspects with that against oxidative stress. After exposure to oxidative stress, the Akt-PI3K signaling and the p38 signaling in the trabecular meshwork cells were revealed to be activated. Moreover, oxidative stress-induced cell death was enhanced by inhibiting these signalings. These novel findings provided us a valuable clue to understanding the mechanisms that regulate aqueous humor outflow.
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Report
(3 results)
Research Products
(52 results)
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[Presentation] 原発隅角閉塞に対する白内障手術併用隅角癒着解離術における眼圧予後不良因子の検討2010
Author(s)
亀田隆範, 井上俊洋, 稲谷大, 中西秀樹, 赤木忠道, 豊川紀子, 熊谷京子, 西脇弘一, 黒田真一郎, 栗本康夫, 吉村長久, 谷原秀信
Organizer
第64回日本臨床眼科学会
Place of Presentation
神戸国際会議場、神戸
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[Presentation] Risk factors of goniosynechialysis combined with phacoemulsification and intraocular lens implantation for treatment of primary angle closure.2010
Author(s)
Kameda T, Inoue T, Inatani M, Nakanishi H, Nakamura H, Yoshimura N, Akagi T, Nishiwaki H, Kumagai K, Kurimoto Y, Tanihara H.
Organizer
28th Congress of the European Society of Cataract & Refractive Surgeons
Place of Presentation
Palais des Congres, Paris, France
Related Report
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[Presentation] Risk Factors for Secondary Glaucoma After Vitrectomy for Proliferative Diabetic Retinopathy.2010
Author(s)
Tanaka A, Inatani M, Inoue T, Kasaoka N, Takihara Y, Ito Y, Fukushima M, Tanihara H.
Organizer
2010 ARVO Annual Meeting
Place of Presentation
Greater Fort Lauderdale/Broward County Convention Center, Fort Lauderdale, Florida, USA
Related Report
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[Presentation] Trabeculectomy With Mitomycin C for Open-Angle Glaucoma in Phakic Eyes vs.Pseudophakic Eyes After Phacoemulsification.2010
Author(s)
Takihara Y, Inatani M, Seto T, Iwao K, Iwao M, Inoue T, Kasaoka N, Murakami A, Futa R, Tanihara H.
Organizer
2010 ARVO Annual Meeting
Place of Presentation
Greater Fort Lauderdale/Broward County Convention Center, Fort Lauderdale, Florida, USA
Related Report
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[Presentation] RhoA/ROCK Pathway Mediated the Expression of Type1 Collagen Induced by TGF-β2 in Trabecular Meshwork Cells.2010
Author(s)
Fujimoto T, Inoue-Mochita M, Inoue T, Ohtsu N, Kameda T, Kasaoka N, Kimoto K, Tanihara H.
Organizer
2010 ARVO Annual Meeting
Place of Presentation
Greater Fort Lauderdale/Broward County Convention Center, Fort Lauderdale, Florida, USA
Related Report
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